MOC-CME

Evidence-Based Medicine: The Evaluation and

Treatment of Pressure Injuries
Joseph A. Ricci, M.D.
Lauren R. Bayer, P.A.-C.
Dennis P. Orgill, M.D., Ph.D.
Boston, Mass.
Learning Objective: After studying this article, the participant should be able
to: 1. Discuss the approach to and rationale for pressure injury management,
including specific techniques for prevention and preoperative evaluation. 2.
Develop a management algorithm for these wounds that includes operative and
nonoperative modalities. 3. Understand how to identify and manage the com-
plications of surgical intervention for pressure injuries, including recurrence.
Summary: Pressure injuries are a common problem associated with great mor-
bidity and cost, often presenting as complex challenges for plastic surgeons.
Although the cause of these wounds is largely prolonged pressure, the true
pathogenesis involves many other factors, including friction, shear, moisture,
nutrition, and infection. This article outlines a systematic approach to evaluating
and staging pressure injuries, and provides strategies for treatment and preven-
tion. Critical to surgical intervention is thorough débridement, including any
involved or causative bony tissues, and postoperative management to prevent
wound dehiscence and recurrence.  (Plast. Reconstr. Surg. 139: 275e, 2017.)

P
ressure injuries date back to antiquity, with
some of the earliest known instances discov-
ered during autopsies of Egyptian mummies.1
Although wound care and surgical intervention
have become increasingly complex, the basic pres-
sure injury management concepts of prevention,
nonoperative treatment, preoperative patient opti-
mization, thorough débridement, and tension-free
soft-tissue coverage remain unchanged.
Precise determination of the incidence and
prevalence of pressure injuries is difficult given
the substantial variation in description and report-
ing across institutions. The overall pressure injury
prevalence rate described in 1999 for acute care
facilities was 14.8 percent, with facility-acquired
pressure injuries accounting for 7.1 percent.2
Despite improvements in treatment and preven-
tion, nearly identical results were obtained by the
same group’s review of the International Pressure
Ulcer Prevalence Survey in 2009.3 Subgroup anal-
ysis demonstrated that the facility-acquired prev-
alence rates were highest in adult intensive care
units, ranging from 8.8 to 12.1 percent.2,3
Particular populations are identified to be
at a higher risk for developing pressure injuries:
From the Division of Plastic Surgery, Brigham and Women’s
Hospital, Harvard Medical School.
Received for publication August 21, 2015; accepted
­December 29, 2015.
Copyright © 2016 by the American Society of Plastic Surgeons
DOI: 10.1097/PRS.0000000000002850
patients with hip fractures (range, 8.8 to 55 per-
cent) and those with spinal cord injuries (range,
33 to 60 percent).4–6 Risk factors for patients with
spinal cord injuries include insensitivity, immobil-
ity, urinary and bowel incontinence, a history of
previous pressure injury, and tobacco use. Elderly
patients with immobility and/or cachexia are also
at risk.7,8 Lower extremity trauma resulting in bone
or soft-tissue injury and subsequent fixation with
casting can result in pressure injuries under the cast
or on the heels. Several studies have identified the
sacrum (28 to 36 percent) as the most common site
to develop a pressure injury, closely followed by the
heel (23 to 30 percent) and the ischium (17 to 20
percent).6,9–11 In patients with spinal cord injuries,
coccygeal pressure injuries occur most commonly
Disclosure: Dr. Orgill is a consultant for Kinetic
Concepts, Inc. The other two authors have no finan-
cial interest to declare in relation to the content of
this article.
Supplemental digital content is available for
this article. Direct URL citations appear in the
text; simply type the URL address into any Web
browser to access this content. Clickable links
to the material are provided in the HTML text
of this article on the Journal’s website (www.
PRSJournal.com).

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 Plastic and Reconstructive Surgery • January 2017
in the acute injury phase, as patients are usually
lying supine. Subsequently, ischial pressure injuries
develop as they begin to sit in a wheelchair.6,9–11
The National Pressure Ulcer Advisory Panel
estimates the cost to treat and heal one hospi-
tal-acquired pressure injury at approximately
$100,000.12 In 2006, the Institute of Healthcare
Improvement estimated the financial burden to
the health care system of managing pressure inju-
ries in nursing homes to be $11 billion.13 Patients
with pressure injuries also burden the system with
increased rates of hospital admission and lengths
of stay compared with patients without pressure
injuries (14.1 days versus 5.0 days).13
PATHOPHYSIOLOGY
Pressure injuries are caused by unrelieved
pressure to the soft tissue over a bony promi-
nence.12 Pressure applied to soft tissue at a level
higher than that found in the blood vessels sup-
plying the area can cause ischemia and edema,
and ultimately pressure injuries. Skin is more
resistant to pressure than muscle, sometimes
masking a deeper injury. Pressure, roughly dou-
ble capillary closing pressure, applied for 2 hours
results in irreversible ischemic damage to tissue,
but pressures below this threshold or for a shorter
duration are unlikely to cause necrosis.14 Current
clinical protocols for repositioning patients every
2 hours are based on these data.
Additional factors to be considered include
friction, shear force, moisture, malnutrition, social
factors, and neurologic injury. Pressure injury
development can be accelerated or enhanced by
friction and moisture. When tissue planes move in
opposite directions, shear force results. Friction is
the force resisting relative motion between two
surfaces. Frictional forces often develop between
a patient’s skin and contact surfaces, such as bed
sheets, sliding boards, and mobility devices such
as wheelchair cushions. Superficial skin injuries
caused by excess friction or shear injuries (e.g.,
abrasions, blisters, or tears) may potentiate pres-
sure-induced damage.15,16 As skin integrity is com-
promised, transepidermal water loss increases and
allows moisture to accumulate.
Moisture increases the coefficient of friction
and promotes adherence to sheets and other con-
tact surfaces, further worsening the damage to tis-
sue.17 Excessive moisture can also cause dermatitis
and small breaks in the skin to occur.18 Excess mois-
ture can have many causes, but urinary and fecal
incontinence are of particular importance in the
cause of pressure injuries. Urinary incontinence
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Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
causes excess moisture and neutralizes the acidic
pH of skin, making it prone to breakdown and
infection. Fecal contamination creates excess
moisture and can introduce a large bacterial load
to the wound. Despite being important clinical
considerations, there is no strong evidence to sup-
port the association of urinary or fecal inconti-
nence with pressure injury formation.19–21
Malnutrition is commonly seen in chronically
ill and debilitated patients and has been docu-
mented to have a clear association with the failure
of pressure injuries to heal.22–24 Other deleterious
effects include the following: negative nitrogen
balance; immunosuppression; and an increased
risk of sepsis, infection, in-hospital mortality, and
prolonged hospital stays.25–27
Important but underappreciated factors
involved in the formation of pressure injuries are
social issues. Many chronically debilitated patients
avoid pressure injuries because they have appropri-
ate care, including pressure relief, cleansing, and
adequate nutrition. A change in social situation
could result in the development of a pressure injury
or an acute worsening of an existing wound. Loss of
family support and inability to obtain regular nurs-
ing care or transition to a different nursing home
could all precipitate the onset of a pressure injury.
STAGING
The most widely accepted pressure injury stag-
ing system was developed by the National Pressure
Ulcer Advisory Panel (Table 1).28,29 Stage 1 and 2
pressure injuries can be treated nonoperatively,
whereas stage 3 and 4 pressure injuries often
require surgical intervention. Patients with sus-
pected deep-tissue pressure injury and unstage-
able pressure injuries should be débrided until
they can be clearly staged, although some will heal
with pressure relief and dressings alone.
PREVENTION AND NONSURGICAL
TREATMENT
Pressure Relief
Despite numerous studies and recommenda-
tions for prevention, the overall rates of pressure
sores have not changed dramatically.30,31 Pressure
injuries is the mainstay of management of at-risk
patients, including repositioning patients every
few hours and special pressure offloading devices
and mattresses.32–34 Although there is insufficient
evidence to recommend a particular pressure-
relief surface, there are theoretical advantages of
improved pressure relief and moisture control.34,35
 Volume 139, Number 1 • Pressure Injuries

Table 1.  National Pressure Ulcer Advisory Panel Staging System for Pressure Injuries
Stage Description Treatment
I Nonblanchable erythema Pressure relief, local wound care
II Partial-thickness loss of dermis Pressure relief, local wound care
III Full-thickness loss: visible subcutaneous fat Pressure relief, local wound care, surgical
(but not bone or muscle) ­débridement
IV Full-thickness loss with exposed bone, tendon, or Pressure relief, local wound care, surgical
muscle ­débridement
Unstageable Full-thickness tissue loss with depth obscured by Sharp débridement to determine proper stage
slough or eschar
Suspected deep Depth unknown: purple or maroon colored area Pressure relief, monitor wound evolution
tissue injury with intact skin likely caused by shear forces

The most commonly used pressure offloading
surfaces are mattresses and wheelchair cushions.
Many of these devices are made of specialized
foam that is contoured to the patient, or they
have multiple small air chambers. Both of these
surfaces are used to evenly distribute pressure
instead of creating pressure points. Pharmacolog-
ically controlling spasticity can improve patient
positioning, weight distribution, and hygiene
and can prevent tension on a healing wound.36
The Braden Scale is the most commonly used
validation tool for predicting patients at risk for
developing pressure injuries and can be used to
develop a pressure injury strategy (Table 2).37
Pressure injuries are now considered among
the eight preventable conditions identified by the
Centers for Medicare & Medicaid Services as “never
events.”38 In 2008, the Centers for Medicare & Med-
icaid Services deemed that hospitals will receive
lower payments related to the injury-specific care of
patients who acquire either a stage 3 or 4 pressure
injury during their hospitalization.38,39 Some pri-
vate insurers have also adopted this reimbursement
scheme. Many hospitals now have implemented
systems to track hospital-acquired pressure injuries,
identifying modifiable risk factors and developing
prevention strategies to decrease patient morbidity
and lost reimbursement.38 Initial outcomes demon-
strate earlier identification, a decrease in the inci-
dence of pressure injuries per 1000 patient days, a
decrease in the rate of admissions caused by pres-
sure injuries, and improved patient outcomes.38
Importantly, however, the labeling of pressure inju-
ries as never events may be inaccurate, as many cli-
nicians caring for pressure injuries feel that not all
pressure injuries are preventable. For instance, even
with proper padding and ideal nursing care, some
very frail patients have developed pressure injuries.
Nutrition Optimization
Although no direct causal relationship has been
established between malnutrition and pressure
injuries, there is a clear association between the
two. Protein, vitamin, and mineral intake should
be optimized, and albumin and prealbumin lev-
els should be checked and trended. Preopera-
tive goals of albumin levels greater than 3  g/dl
and prealbumin levels greater than 20 mg/dl are
recommended before performing elective flap cov-
erage of a pressure injury. Low serum prealbumin
predicts a poor prognosis for wound healing.40,41
There is little evidence to support an association
between other micronutrients (vitamin C or zinc)
with pressure injuries and in the absence of a spec-
ified deficiency state.42,43 One exception is vitamin
A supplementation, which has demonstrated util-
ity in patients taking corticosteroids.44,45
Patients with pressure injuries should undergo
evaluation by a nutritionist and calorie counts
if indicated to help determine whether they are
receiving adequate nutrition. Vitamin supplements
and high-protein diets can be devised and their
administration can be supervised by the nutrition
staff. In rare cases, tube feeds through a gastros-
tomy or jejunostomy tube can be considered if the
patient is not meeting their dietary goals by mouth.
Infection
Wound infection should be diagnosed and
treated aggressively to avoid a necrotizing infec-
tion. Osteomyelitis is a common complication of
pressure injuries and mandates operative débride-
ment and culture-directed antibiotic and therapy.46
Traditional therapy for osteomyelitis is 6 weeks of
intravenous antibiotic therapy, but shorter courses
may be effective.7,47 Soft-tissue infections with
open, draining wounds can be treated with wound
care and antibiotics alone. Deep pressure injury
tracts can become walled off, causing an abscess,
requiring prompt surgical drainage, followed by
culture-directed antibiotics. Deep tissue cultures
taken in the operating room after débridement
are preferable to wound swabs (which may rep-
resent necrotic tissue and contaminants) or bone

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Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
 Table 2.  Braden Score for Evaluating Pressure Sore Risk*

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Score
1 2 3 4
Sensory Ability to Completely Limited Very Limited Slightly Limited No Impairment
perception respond Unresponsive (does not moan, Responds only to painful stimuli. Responds to verbal commands, Responds to verbal com-
meaning- flinch, or grasp) to painful Cannot communicate discom- but cannot always communi- mands. Has no sensory
fully stimuli, because of diminished fort except by moaning or cate discomfort or the need deficit which would limit
to pressure- level of consciousness or seda- restlessness or has a sensory to be turned or has some ability to feel or voice pain
related tion or limited ability to feel pain impairment which limits the sensory impairment which or discomfort.
discomfort over most of body. ability to feel pain or discomfort limits ability to feel pain or
over half of body. discomfort in one or two
extremities.
Moisture Degree to Constantly Moist Very Moist Occasionally Moist Rarely Moist
which skin is Skin is kept moist almost constantly Skin is often, but not always moist. Skin is occasionally moist, Skin is usually dry; linen
exposed to by perspiration, urine, etc. Linen must be changed at least requiring an extra linen only requires changing at
moisture Dampness is detected every time once a shift. change approximately once routine intervals.
patient is moved or turned. a day.
Activity Degree of Bedfast Chairfast Walks Occasionally Walks Frequently
physical Confined to bed. Ability to walk severely limited or Walks occasionally during day, Walks outside room at least
activity nonexistent. Cannot bear own but for very short distances, twice a day and inside
weight and/or must be assisted with or without assistance. room at least once every
into a chair or wheelchair. Spends majority of each shift 2 hr during waking hours.
in bed or chair.
Mobility Ability to Completely Immobile Very Limited Slightly Limited No Limitation
change and Does not make even slight changes Makes occasional slight changes in Makes frequent though slight Makes major and frequent
control body in body or extremity position body or extremity position but changes in body or extremity changes in position with-
position without assistance. unable to make frequent or sig- position independently. out assistance.
nificant changes independently.
Nutrition Usual food Very Poor Probably I­ nadequate Adequate Excellent
intake Never eats a complete meal. Rarely Rarely eats a complete meal and Eats over half of most meals. Eats most of every meal.
pattern eats more than half of any food generally eats only approxi- Eats a total of four servings of Never refuses a meal. Usu-
offered. Eats two servings or less mately two of any food offered. protein (meat, dairy prod- ally eats a total of four or
of protein (meat or dairy prod- Protein intake includes only ucts) per day. Occasionally more servings of meat and
ucts) per day. Takes fluids poorly. three servings of meat or dairy will refuse a meal, but will dairy products. Occasion-
Does not take a liquid dietary products per day. Occasionally usually take a supplement ally eats between meals.
supplement or is NPO and/or will take a dietary supplement when offered or is on a tube Does not require supple-
maintained on clear liquids or IV or receives less than optimum feeding or TPN regimen that mentation.
fluids for more than 5 days. amount of tube feeds. probably meets most needs.
Friction and Problem Potential Problem No Apparent Problem Total score†
shear Requires moderate to maximum Moves feebly or requires mini- Moves in bed and in chair
assistance in moving. Complete mum assistance. During a move independently and has suf-
lifting without sliding against skin probably slides to some ficient muscle strength to lift
sheets is impossible. Frequently extent against sheets, chair, up completely during move.
slides down in bed or chair, restraints, or other devices. Maintains good position in
requiring frequent repositioning Maintains relatively good posi- bed or chair.
with maximum assistance. Spas- tion in chair or bed most of
ticity, contractures, or agitation the time but occasionally slides
leads to almost constant friction. down.
NPO, nothing by mouth; IV, intravenous; TPN, total parenteral nutrition.
*Each category is scored from 1 to 4, with the “friction and shear category” only scored from 1 to 3. These combine for a possible total of 23 points, with a higher score meaning a lower risk
of developing a pressure injury.
Plastic and Reconstructive Surgery • January 2017

†Total score: very high risk, total score 9 or less; high risk, total score of 10–12; moderate risk, total score of 13–14; mild risk, total score of 15–18; and no risk, total score of 19–23.

Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
 Volume 139, Number 1 • Pressure Injuries
biopsies alone. Our institution avoids performing
bone biopsies alone, without complete débride-
ment, amid concerns over the risk of seeding a
localized infection into uninvolved bone.
Wound Care
Many pressure injuries heal without surgery,
by means of pressure relief, risk factor correc-
tion, and appropriate wound treatment. Non-
surgically optimizing the tissues and wound size
will afford a smaller, less complex operation in
the future. Local wound care clears the wound of
debris, absorbs drainage, facilitates the formation
of granulation tissue, and stimulates wound con-
traction. There are a countless number of wound
care products, with little evidence to recommend
one dressing over others.48 A meta-analysis of
the various dressings and topical agents used for
pressure injury treatment failed to find any sig-
nificant differences among available products.48
Mechanical débridement of necrotic tissue can
be accomplished, using saline- or Dakin’s-damp-
ened gauze packed into the wound, in addition to
sharp débridement. Other débridement modali-
ties include high-pressure irrigation, enzymatic
débridement with collagenase, mānuka honey,
and certain foam dressings. Often, sharp débride-
ment is required before a trial of local wound care
with dressings including negative-pressure wound
therapy. Once the wound is free of devitalized tis-
sue, the full extent of the wound can be examined
and more accurate staging performed.
Dressings should be chosen based on char-
acteristics of the wound, ease of use, specific
function, and cost.49 Occlusive films and hydro-
colloids are frequently used on dry, shallow
pressure injuries, whereas alginates and other
Fig. 1. Typical results of pressure injuries treated with negative-pressure wound therapy. (Left) Initial ischial pressure
injury. (Right) After 2 months of treatment, the injury is now ready for closure. Note the contracture of the wound,
proliferation of granulation tissue, and removal of slough.
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
absorbent dressings are for deeper, heavily exu-
dative wounds.49 Individual products within the
same class may differ widely in their capacity for
absorption, occlusion, permeability, and cohe-
sion.49 Numerous topical agents are used for
decreasing bacterial burden and for wound heal-
ing.48 Mafenide, acetic acid, Dakin’s solution, and
iodine preparations have been documented to
kill fibroblasts and bacteria, potentially impeding
wound healing with prolonged use, and should
be reserved for instances of active infection or
large amounts of necrotic tissue.50,51 Silver sulfa-
diazine and other silver agents have been dem-
onstrated to be toxic to fibroblasts, but to a lesser
degree. Dressings formulated with silver ions
are often well tolerated and commonly used.52,53
Several large reviews of these products have not
found convincing data to support the use of any
particular topical agent.35
The use of negative-pressure wound therapy
has had a significant impact on the treatment
of pressure injuries (Fig.  1). Negative-pressure
wound therapy increases granulation tissue
by applying microdeformational forces to the
wound bed and can be used to manage exudate
and bacterial burden and assist in wound con-
traction.54 Preoperative use can shrink the size
of a large wound, facilitating a smaller surgical
flap closure. Negative-pressure wound therapy
should be avoided in the presence of necrotic tis-
sue and negative-pressure wound therapy should
be stopped if the wound deteriorates. The use of
other biophysical treatments such as hyperbaric
oxygen therapy, electrical stimulation, noncon-
tact ultrasound, and phototherapy are controver-
sial, and more studies are required to determine
their efficacy.55
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 Plastic and Reconstructive Surgery • January 2017

SURGICAL TREATMENT to demarcate the margins of the bursa and tracks

Basic surgical principles for the treatment of
pressure injuries include complete excision of the
wound, including all devitalized tissue, scar, and
bursa; removal of underlying or exposed bone;
padding of any remaining bony prominences; fill-
ing dead space; resurfacing the wound with large
regional pedicled flaps; and using skin grafts, if
necessary, to close the donor site. Flaps should be
designed as large as possible, placing the suture
line away from the area of direct pressure. The
flap design should not violate adjacent flap ter-
ritories and should allow for readvancement or
rerotation to preserve future coverage options if
needed after a recurrence.
Surgical Débridement
Chronic pressure injuries may have a relatively
well-defined bursa in continuity with the base of
the wound and thus methylene blue can be applied
(Fig. 2). The entire wound and surrounding scar
tissues and heterotopic ossification are removed,
leaving only healthy tissue (Fig.  3). Prominent,
devitalized, or infected bone is removed with an
osteotome or rongeur to ensure that healthy, hard,
bleeding bone is all that remains (Fig. 4). A deep
bone culture can be taken to identify any true
pathogens, and all tissue should be sent for Gram
stain, culture, and pathologic assessment. Thor-
ough débridement should never be compromised
to facilitate wound closure, as incomplete débride-
ment is a common cause of flap failure and wound
recurrence. Postoperative antibiotic therapy
should be guided by the results of deep intraop-
erative bone cultures.56 (See Video, Supplemental
Digital Content 1, which demonstrates treatment
of a left ischial pressure injury. Dr. Orgill retains
copyright on this video. This video is available in
the “Related Videos” section of the full-text article

Fig. 2. (Left) Preoperative photograph of a patient with sacral and ischial pressure injuries. (Right) Wounds are marked
with methylene blue on cotton swabs to identify entire bursa.

Fig. 3. (Left) Intraoperative and (right) postoperative photographs of complete en bloc resection of pressure injury
bursa that is identified with methylene blue dye.

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Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
 Volume 139, Number 1 • Pressure Injuries
Fig. 4. Routine use of an osteotome to remove any prominent
bone, any infected bone, or any bone at the base of the bursa.
Video 1. Supplemental Digital Content 1 demonstrates treat-
ment of a left ischial pressure injury. Dr. Orgill retains copyright
on this video. This video is available in the “Related Videos” sec-
tion of the full-text article on PRSJournal.com or at http://links.
lww.com/PRS/B943.
on PRSJournal.com or at http://links.lww.com/PRS/
B943.)
Options for Closure
Common options for surgical closure after
complete débridement include the following:
pedicled muscle, myocutaneous, or fasciocutane-
ous flaps and, less commonly, free flaps (Table 3).
Primary closure is rarely recommended unless the
defect is very small. Skin grafting does not offer
sufficient long-term durability, and failure rates
are high.7 The choice of coverage depends on
the location of the wound, the need for ambula-
tion, a history of prior pressure injury, previous
surgical interventions, and comorbidities. Use
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
Table 3.  Common Coverage Options for Commonly
Encountered Pressure Injuries
Anatomical Site Commonly Used Options for Closure
Sacral Gluteal myocutaneous flap
Gluteal fasciocutaneous rotation-
advancement flap
Gluteal fasciocutaneous V-Y advancement
flap
Superior gluteal artery perforator flap
Ischial Inferior gluteal myocutaneous flap
Gracilis myocutaneous flap
Biceps femoris (hamstring)
myocutaneous flap
Lateral thigh fasciocutaneous flap
Anterolateral thigh fasciocutaneous flap
Rectus abdominis myocutaneous flap
Inferior gluteal artery perforator flap
Profunda femoris artery perforator flap
Trochanteric Tensor fasciae latae myocutaneous flap
(bipedicle or V-Y types)
Vastus lateralis myocutaneous flap
Expansive gluteal myocutaneous flap
Anterolateral thigh perforator flap
Foot/ankle Reverse sural artery flap
Medial plantar flap
Extensor digitorum brevis flap
Propeller flaps
Free tissue transfer
of a myocutaneous flap for closure of a pressure
injury has the advantage of greater bulk for filling
the wound cavity and obliterating dead space.57,58
However, fasciocutaneous flaps can preserve
the muscle (and its function), conserve future
reconstructive options, and adhere to principle
of placing suture lines away from areas of direct
pressure.59 Use of fasciocutaneous flaps is critical
in ambulatory patients or those who can indepen-
dently transfer themselves, to preserve muscle
function.59 Free flaps are rarely used except when
indicated to provide a sensate flap, lower extremity
flap, or when multiple adjacent pressure injuries
require coverage. Table  3 outlines several com-
mon coverage options for the more commonly
encountered pressure injuries, although this is
by no means an exhaustive list of all the options.
It is important to note that every pressure injury
operations should be planned to allow for the pos-
sibility of future secondary procedures, if needed.
Ischial
The ischial tuberosity presents the most sig-
nificant source of pressure to patients who sit
for extended periods without shifting position.
Choices for coverage of ischial defects are the
gluteal myocutaneous flap, the V-Y hamstring
advancement, the medial thigh and, less com-
monly, the gracilis flap (Table  3). Fasciocutane-
ous flaps, such as the tensor fascia lata and gluteal
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 Plastic and Reconstructive Surgery • January 2017
Fig. 5. Example of a fasciocutaneous flap advanced in V-Y fash-
ion for closure of a right trochanteric wound. Short-term follow-
up is shown.
thigh flap, often lack sufficient bulk to fill the dead
space. Gluteal flaps can be either a myocutaneous
or muscle-only flap and should be designed as an
advancement or rotation flap.7,8,47 The hamstring
advancement flap can be used to provide signifi-
cant bulk with the incorporation of the biceps
femoris, semitendinosus, and semimembranosus
muscles. Drawbacks of the hamstring flap include
tension at the closure, suture lines directly over
pressure points, and potential dehiscence with
flexion at the hip joint.
Critical to the treatment of these wounds is
avoidance of prolonged sitting. Many of these
patients often return to their preoperative sitting
habits, leading to a high rate of recurrence. Mini-
mizing local tissue disruption allows for future
flap design. Both gluteal and hamstring flaps
can be readvanced multiple times, making them
extremely useful for treating recurrent wounds.
Trochanteric
Trochanteric pressure injuries are most com-
monly found among patients who stay in the lat-
eral decubitus position, often a result of spasticity
Fig. 6. (Left) Initial sacral pressure injury, (center) after débridement, and (right) after closure using a fasciocutaneous gluteal V-Y
advancement on the left side and a gluteal advancement rotation on the right side.
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Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
of the lower extremity or hip flexion contractures.
Treatment of contractures and spasticity should
be considered before reconstruction. A tensor fas-
ciae latae flap can be raised in a bipedicle or as a
V-Y flap (Fig. 5). The T12 to L3 sensory input to
this flap makes it useful for patients with a lower
level spinal cord injury, potentially allowing for
postoperative sensation at the site of the wound
to prevent recurrence. These flaps are ideal for
shallow trochanteric wounds or can be taken with
the vastus lateralis or rectus femoris if the wound
is deeper.
Sacral
Sacral pressure injuries are managed similar
to ischial defects, and gluteal flaps represent the
workhorse flap for closure. They can be raised
as myocutaneous or muscle-only flaps and can
be advanced into a flap either by rotation or in
V-Y fashion. Both versions are reliable and can
be readvanced for a recurrence. Larger defects
may require bilateral flaps (Fig.  6). In ambula-
tory patients, gluteal fasciocutaneous flaps may be
used to preserve ambulation and core strength.
Less common alternatives include the transverse
and vertical lumbosacral flap, based on lumbar-
perforating vessels, but they lack significant bulk
and are not useful in deeper wounds.
Lower Extremity (Heel and Ankle)
Wounds of the lower extremity can occur from
prolonged supine positioning and in patients with
lower extremity injuries who develop pressure
injuries from tight casts or splints. Reconstruction
is challenging because of the limited amount of
locally available, mobile soft tissue. Commonly
used local options include a reverse sural artery
flap for wounds over the medial or lateral mal-
leolus. Reliability of this flap can be improved by
staging the reconstruction with a surgical delay.
 Volume 139, Number 1 • Pressure Injuries
Fig. 7. (Left) Pressure injury on the lateral malleolus with perforator-based propeller flap marked adjacent and (center) closure
of wound by rotation of flap and skin grafting of the donor site to avoid undue tension on the closure. (Right) Several weeks
postoperatively.
Propeller flaps can cover many ankle wounds if
acceptable perforators are identified (Fig. 7).
Plantar foot wounds can be covered with the
medial plantar flap providing glabrous skin from
the instep to recreate the plantar walking surface.
Skin grafts will not suffice in this area and will
likely experience breakdown over time. Free tis-
sue transfer with an anterolateral thigh or radial
forearm flap can be used to obtain coverage for
any lower extremity wound, particularly when
located in the distal third of the lower leg.
POSTOPERATIVE CONSIDERATIONS
Postoperative management has been exten-
sively reviewed in the literature and includes the
preoperative protocols instituted before surgery,
including relief of pressure, shear, friction, and
moisture; good skin care; incontinence and spas-
ticity control; smoking cessation; and nutritional
supplementation.60–63 Support surfaces should be
reevaluated for even pressure distribution. Ide-
ally, pressures should be no more than 35 mmHg
for immobile patients and 60 mmHg for those
who can relieve pressure by lifting or leaning.64
The patient, family, social support, and care team
must be prepared and in agreement on the post-
operative care plan and all support services put
in place before surgery. If there is not enough
social support at home, including 24-hour care,
inpatient rehabilitation or skilled nursing facility
stay is recommended. Duration of bedrest and
the time to starting sitting protocols and physical
therapy are critical. Patients with pelvic pressure
injuries are kept in bed for 6 to 8 weeks based on
data indicating that wounds reached maximum
tensile strength after this period.65,66 Although
recent studies advocate a more rapid sitting pro-
gression, patients may benefit from 6 weeks of
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
complete pressure relief on a pressure-relieving
mattress and repositioning every 2 to 4 hours.67
Active and passive range-of-motion exercises of
the uninvolved extremity can begin early in the
postoperative course, and the affected extremity
can be ranged after the initiation of a sitting pro-
tocol once the incision is well healed.65,67
After the period of offloading, patients may sit
up in bed for 15 minutes at a time, up to three
times per day initially. If the incision and flap are
free from erythema, induration, or drainage, sit-
ting in a chair with a pressure-relieving cushion
may begin. Sitting time then increases in 15-min-
ute increments every 2 to 3 days with the goal of 2
hours each time after 2 weeks. If there is evidence
of wound breakdown, sitting must be stopped
immediately and restarted back at the beginning
once the wound has healed again. Patients should
follow up monthly for at least 3 months and then
every 3 to 6 months to reinforce pressure injury
prevention strategies and identify any skin areas
of concern. For lower extremity flaps, specific
institutional protocols for activity progression
should be followed.
The most common postoperative complica-
tions of pressure injury surgery include hema-
toma, seroma, infection, and wound dehiscence.
However, recurrence remains the most important
complication. A small breakdown in the suture
line should heal with local wound care and pres-
sure relief. Any persistent wound dehiscence or
late developing wound may indicate pressure-
related recurrence (Fig. 8). The true incidence of
pressure injury recurrence is difficult to quantify
because of the lack of long-term outcome studies.
The available literature reports a widely variable
rate of recurrence ranging from as low as 3 to 6
percent to as high as 33 to 100 percent.63,65,68,69 Sev-
eral studies have reported higher recurrence rates
283e
 Plastic and Reconstructive Surgery • January 2017
Fig. 8. Patient shown in Figure 7 with a propeller flap to the lat-
eral malleolus with early recurrent ulceration several months
after complete closure has been achieved.
Video 2. Supplemental Digital Content 2 shows an interview with
a 38-year-old quadriplegic patient discussing avoidance of pres-
sure injuries. Dr. Donald H. Lalonde retains copyright on this video.
This video is available in the “Related Videos” section of the full-text
article on PRSJournal.com or at http://links.lww.com/PRS/B944.
in paraplegic patients (82 percent at 18 months)
compared with nonparaplegic patients.70
Recurrent pressure injuries can be reoper-
ated on, but the patient must be fully reevalu-
ated to control any risk factors that might have
led to the recurrence. A previous flap can be
readvanced, eliminating all tension by a change
of plane (e.g., by advancing a fasciocutaneous
flap over a previous myocutaneous flap). If there
has been prior flap advancement or if the tissue
is of poor quality because of recurrent injuries or
scarring, a flap from a new anatomical area can
be used. Amputation remains an option for some
patients with multiple episodes of recurrence,
284e
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
or where the wound is extensive to the point of
precluding closure with standard flaps, or for
patients who are severely ill because of uncon-
trollable infection.71,72 (See Video, Supplemen-
tal Digital Content 2, which shows an interview
with a 38-year-old quadriplegic patient discuss-
ing avoidance of pressure injuries. Dr. Donald
H. Lalonde retains copyright on this video. This
video is available in the “Related Videos” section
of the full-text article on PRSJournal.com or at
http://links.lww.com/PRS/B944.)
CONCLUSIONS
Despite improvements in prevention and
advances in surgical and nonsurgical manage-
ment, pressure injuries remain a formidable prob-
lem for medical practitioners. With the recent
inclusion of pressure injuries on the list of never
events for hospitalized patients, study of preven-
tion and treatment should continue. Optimizing
the entire medical and social condition of the
patient and providing consistent pressure relief
are critical adjuncts to advanced wound therapies
and successful surgical outcomes. A thorough
understanding of the available literature will help
plastic surgeons to not only treat these compli-
cated wounds but possibly prevent their forma-
tion as well.
Dennis P. Orgill, M.D., Ph.D.
Division of Plastic Surgery
Brigham and Women’s Hospital
75 Francis Street
Boston, Mass. 02115
dorgill@partners.org
REFERENCES
1. Rowling JT. Pathological changes in mummies. Proc R Soc
Med. 1961;54:409–415.
2. Amlung SR, Miller WL, Bosley LM. The 1999 National
Pressure Ulcer Prevalence Survey: A benchmarking
approach. Adv Skin Wound Care 2001;14:297–301.
3. VanGilder C, Amlung S, Harrison P, Meyer S. Results of the
2008-2009 International Pressure Ulcer Prevalence Survey
and a 3-year, acute care, unit-specific analysis. Ostomy Wound
Manage. 2009;55:39–45.
4. Baumgarten M, Margolis D, Berlin JA, et al. Risk factors for
pressure ulcers among elderly hip fracture patients. Wound
Repair Regen. 2003;11:96–103.
5. Lindholm C, Sterner E, Romanelli M, et al. Hip fracture
and pressure ulcers: The Pan-European Pressure Ulcer
Study. Intrinsic and extrinsic risk factors. Int Wound J.
2008;5:315–328.
6. Gélis A, Dupeyron A, Legros P, Benaïm C, Pelissier J, Fattal C.
Pressure ulcer risk factors in persons with spinal cord injury
part 2: The chronic stage. Spinal Cord 2009;47:651–661.
7. Cushing CA, Phillips LG. Evidence-based medicine: Pressure
sores. Plast Reconstr Surg. 2013;132:1720–1732.
 Volume 139, Number 1 • Pressure Injuries
8. Bauer J, Phillips LG. MOC-PSSM CME article: Pressure sores.
Plast Reconstr Surg. 2008;121(Suppl):1–10.
9. Dansereau JG, Conway H. Closure of decubiti in paraplegics:
Report of 2000 cases. Plast Reconstr Surg. 1964;33:474–480.
10. Meehan M. National pressure ulcer prevalence survey. Adv
Wound Care 1994;7:27–30, 34, 36.
11. Fuhrer MJ, Garber SL, Rintala DH, Clearman R, Hart KA.
Pressure ulcers in community-resident persons with spi-
nal cord injury: Prevalence and risk factors. Arch Phys Med
Rehabil. 1993;74:1172–1177.
12. Description of NPUAP. National Pressure Ulcer Advisory
Panel. Adv Wound Care 1995;8(Suppl):93–95.
13. Russo CA, Steiner C, Spector W. Hospitalizations related
to pressure ulcers among adults 18 years and older, 2006:
Statistical brief #64. In: Healthcare Cost and Utilization
Project (HCUP) Statistical Briefs. Rockville, Md.; Agency for
Healthcare Research and Quality; 2006.
14. Dinsdale SM. Decubitus ulcers: Role of pressure and friction
in causation. Arch Phys Med Rehabil. 1974;55:147–152.
15. Gerhardt LC, Mattle N, Schrade GU, Spencer ND, Derler
S. Study of skin-fabric interactions of relevance to decubi-
tus: Friction and contact-pressure measurements. Skin Res
Technol. 2008;14:77–88.
16. Hanson D, Langemo DK, Anderson J, Thompson P, Hunter
S. Friction and shear considerations in pressure ulcer devel-
opment. Adv Skin Wound Care 2010;23:21–24.
17. Gerhardt LC, Strässle V, Lenz A, Spencer ND, Derler
S. Influence of epidermal hydration on the friction
of human skin against textiles. J R Soc Interface 2008;5:
1317–1328.
18. Defloor T, Grypdonck MF. Validation of pressure ulcer
risk assessment scales: A critique. J Adv Nurs. 2004;48:
613–621.
19. Brandeis GH, Morris JN, Nash DJ, Lipsitz LA. The epidemi-
ology and natural history of pressure ulcers in elderly nurs-
ing home residents. JAMA 1990;264:2905–2909.
20. Cakmak SK, Gül U, Ozer S, Yiğit Z, Gönü M. Risk factors for
pressure ulcers. Adv Skin Wound Care 2009;22:412–415.
21. Guralnik JM, Harris TB, White LR, Cornoni-Huntley JC.
Occurrence and predictors of pressure sores in the National
Health and Nutrition Examination survey follow-up. J Am
Geriatr Soc. 1988;36:807–812.
22. Casey J, Flinn WR, Yao JS, Fahey V, Pawlowski J, Bergan JJ.
Correlation of immune and nutritional status with wound
complications in patients undergoing vascular operations.
Surgery 1983;93:822–827.
23. Dickhaut SC, DeLee JC, Page CP. Nutritional status:
Importance in predicting wound-healing after amputation.
J Bone Joint Surg Am. 1984;66:71–75.
24. Kay SP, Moreland JR, Schmitter E. Nutritional status and
wound healing in lower extremity amputations. Clin Orthop
Rel Res. 1987;217:253–256.
25. Cuthbertson D. Nutrition in relation to trauma and surgery.
Prog Food Nutr Sci. 1975;1:263–287.
26. Arnold M, Barbul A. Nutrition and wound healing. Plast
Reconstr Surg. 2006;117(Suppl):42S–58S.
27. Wilmore DW, Aulick LH. Systemic responses to injury and the
healing wound. JPEN J Parenter Enteral Nutr. 1980;4:147–151.
28. Black J, Baharestani MM, Cuddigan J, et al.; National
Pressure Ulcer Advisory Panel. National Pressure Ulcer
Advisory Panel’s updated pressure ulcer staging system. Adv
Skin Wound Care 2007;20:269–274.
29. National Pressure Ulcer Advisory Panel. Pressure ulcer
stages. Available at: http://www.npuap.org/resources/edu-
cational-and-clinical-resources/npuap-pressure-ulcer-stages-
categories. Accessed October 27, 2016.
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
30. Vangilder C, Macfarlane GD, Meyer S. Results of nine inter-
national pressure ulcer prevalence surveys: 1989 to 2005.
Ostomy Wound Manage. 2008;54:40–54.
31. Gunningberg L, Stotts NA. Tracking quality over time:
What do pressure ulcer data show? Int J Qual Health Care
2008;20:246–253.
32. Goldstone LA, Norris M, O’Reilly M, White J. A clinical trial
of a bead bed system for the prevention of pressure sores in
elderly orthopaedic patients. J Adv Nurs. 1982;7:545–548.
33. Hofman A, Geelkerken RH, Wille J, Hamming JJ, Hermans
J, Breslau PJ. Pressure sores and pressure-decreasing mat-
tresses: Controlled clinical trial. Lancet 1994;343:568–571.
34. McInnes E, Bell-Syer SE, Dumville JC, Legood R, Cullum
NA. Support surfaces for pressure ulcer prevention. Cochrane
Database Syst Rev. 2008;4:CD001735.
35. Reddy M, Gill SS, Kalkar SR, Wu W, Anderson PJ, Rochon
PA. Treatment of pressure ulcers: A systematic review. JAMA
2008;300:2647–2662.
36. Ferido T, Habel M. Spasticity in head trauma and CVA
patients: Etiology and management. J Neurosci Nurs.
1988;20:17–22.
37. Baris N, Karabacak BG, Alpar ŞE. The use of the Braden
Scale in assessing pressure ulcers in Turkey: A systematic
review. Adv Skin Wound Care 2015;28:349–357.
38. Zaratkiewicz S, Whitney JD, Lowe JR, Taylor S, O’Donnell
F, Minton-Foltz P. Development and implementation of a
hospital-acquired pressure ulcer incidence tracking system
and algorithm. J Healthc Qual. 2010;32:44–51.
39. Mattie AS, Webster BL. Centers for Medicare and Medicaid
Services’ “never events”: An analysis and recommendations
to hospitals. Health Care Manag (Frederick) 2008;27:338–349.
40. Evans E. Nutritional assessment in chronic wound care.
J Wound Ostomy Continence Nurs. 2005;32:317–320.
41. Perry D, Borchert K, Burke S, et al.; Institute for Clinical Systems
Improvement. Pressure Ulcer Prevention and Treatment Protocol. 3rd
ed. Updated January 2012. Available at: https://www.icsi.org/_
asset/6t7kxy/PressureUlcer.pdf. Accessed May 5, 2015.
42. Doley J. Nutrition management of pressure ulcers. Nutr Clin
Pract. 2010;25:50–60.
43. Langer G, Fink A. Nutritional interventions for prevent-
ing and treating pressure ulcers. Cochrane Database Syst Rev.
2014;6:CD003216.
44. Hunt TK. Vitamin A and wound healing. J Am Acad Dermatol.
1986;15:817–821.
45. Wicke C, Halliday B, Allen D, et al. Effects of steroids and
retinoids on wound healing. Arch Surg. 2000;135:1265–1270.
46. Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: A
review of clinical features, therapeutic considerations
and unusual aspects (second of three parts). N Engl J Med.
1970;282:260–266.
47. Bauer JD, Mancoll JS, Phillips LG. Pressure sores. In:
Grabb WC, Smith JC, eds. Grabb and Smith’s Plastic Surgery.
6th ed. Philadelphia: Lippincott Williams & Wilkins;
2007:722–729.
48. Bradley M, Cullum N, Nelson EA, Petticrew M, Sheldon T,
Torgerson D. Systematic reviews of wound care manage-
ment: (2). Dressings and topical agents used in the healing
of chronic wounds. Health Technol Assess. 1999;3:1–35.
49. Lionelli GT, Lawrence WT. Wound dressings. Surg Clin North
Am. 2003;83:617–638.
50. Kjolseth D, Frank JM, Barker JH, et al. Comparison of the
effects of commonly used wound agents on epithelialization
and neovascularization. J Am Coll Surg. 1994;179:305–312.
51. Lineaweaver W, McMorris S, Soucy D, Howard R. Cellular
and bacterial toxicities of topical antimicrobials. Plast
Reconstr Surg. 1985;75:394–396.
285e
 Plastic and Reconstructive Surgery • January 2017
52. Geronemus RG, Mertz PM, Eaglstein WH. Wound healing:
The effects of topical antimicrobial agents. Arch Dermatol.
1979;115:1311–1314.
53. Tredget EE, Shankowsky HA, Groeneveld A, Burrell R.
A matched-pair, randomized study evaluating the effi-
cacy and safety of Acticoat silver-coated dressing for the
treatment of burn wounds. J Burn Care Rehabil. 1998;19:
531–537.
54. Orgill DP, Bayer LR. Negative pressure wound therapy:
Past, present and future. Int Wound J. 2013;10(Suppl 1):
15–19.
55. Korzendorfer H, Hettrick H. Biophysical technologies for
management of wound bioburden. Adv Wound Care (New
Rochelle) 2014;3:733–741.
56. Schiffman J, Golinko MS, Yan A, Flattau A, Tomic-Canic M,
Brem H. Operative debridement of pressure ulcers. World J
Surg. 2009;33:1396–1402.
57. Conway H, Griffith BH. Plastic surgery for closure of decu-
bitus ulcers in patients with paraplegia; based on experience
with 1,000 cases. Am J Surg. 1956;91:946–975.
58. Mathes SJ, Alpert BS, Chang N. Use of the muscle flap in
chronic osteomyelitis: Experimental and clinical correlation.
Plast Reconstr Surg. 1982;69:815–829.
59. Higgins JP, Orlando GS, Blondeel PN. Ischial pressure sore
reconstruction using an inferior gluteal artery perforator
(IGAP) flap. Br J Plast Surg. 2002;55:83–85.
60. Disa JJ, Carlton JM, Goldberg NH. Efficacy of operative
cure in pressure sore patients. Plast Reconstr Surg. 1992;89:
272–278.
61. Hentz VR. Management of pressure sores in a specialty cen-
ter: A reappraisal. Plast Reconstr Surg. 1979;64:683–691.
286e
Copyright © 2016 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
62. Stal S, Serure A, Donovan W, Spira M. The perioperative
management of the patient with pressure sores. Ann Plast
Surg. 1983;11:347–356.
63. Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure sores.
Curr Probl Surg. 1977;14:1–62.
64. Dover H, Pickard W, Swain I, Grundy D. The effectiveness
of a pressure clinic in preventing pressure sores. Paraplegia
1992;30:267–272.
65. Minami RT, Mills R, Pardoe R. Gluteus maximus myocuta-
neous flaps for repair of pressure sores. Plast Reconstr Surg.
1977;60:242–249.
66. Levenson SM, Geever EF, Crowley LV, Oates JF III, Berard
CW, Rosen H. The healing of rat skin wounds. Ann Surg.
1965;161:293–308.
67. Kierney PC, Engrav LH, Isik FF, Esselman PC, Cardenas DD,
Rand RP. Results of 268 pressure sores in 158 patients man-
aged jointly by plastic surgery and rehabilitation medicine.
Plast Reconstr Surg. 1998;102:765–772.
68. Ger R, Levine SA. The management of decubitus ulcers by
muscle transposition: An 8-year review. Plast Reconstr Surg.
1976;58:419–428.
69. Relander M, Palmer B. Recurrence of surgically treated pres-
sure sores. Scand J Plast Reconstr Surg Hand Surg. 1988;22:89–92.
70. Evans GR, Dufresne CR, Manson PN. Surgical correction
of pressure ulcers in an urban center: Is it efficacious? Adv
Wound Care 1994;7:40–46.
71. Rubayi S, Ambe MK, Garland DE, Capen D. Heterotopic ossifi-
cation as a complication of the staged total thigh muscles flap
in spinal cord injury patients. Ann Plast Surg. 1992;29:41–46.
72. Niazi ZB, Salzberg CA. Operative repair of pressure ulcers.
Clin Geriatr Med. 1997;13:587–597.