17
CHAPTER
Pressure Sores
Wesley T Myers and Linda G Phillips
Summary
1. In the most widely accepted classification system, pressure
sores are classified according to their tissue depth and the
pathophysiologic changes in the tissue; high-grade pressure
sores (stages III and IV) are indications for surgical
reconstruction.
2. Debridement provides a means of preparing a healthy wound
bed and promotes wound healing. Wound-bed preparation
converts the chronic pressure sore into an acute wound with a
more favorable wound healing environment. All nonviable
tissue, nonviable scar, and infected tissue are removed by
sharp, enzymatic, or mechanical debridement.
3. The main objective in placing a dressing on a pressure sore is
to maintain a moist wound healing environment to facilitate
re-epithelialization and prevent desiccation.
4. Topical antimicrobials are used for pressure sores if the
bacterial count is greater than or equal to 106 CFU/g of soft
tissue or for any level of β-hemolytic streptococci. Bacterial
balance is ultimately controlled by irrigation, debridement, and
closure of the pressure sore.
5. The two categories of surgical intervention are promotion of
the healing process and definitive closure, and surgical options
aim to provide adequate tissue to fill the defect and relieve
pressure from the bony prominence and include
musculocutaneous flaps.
6. Common flap closures for ischial pressure sores, which are the
most frequently encountered pressure sores in paraplegic
patients, include the gluteus maximus in its entirety or as an
island flap, the inferior gluteal thigh flap (IGT), and the V-Y
hamstring flap.
7. Flap selection for coverage of sacral pressure sores relies
heavily upon the gluteus maximus musculocutaneous flap.
Options include the V-Y gluteus maximus flap and buttocks
rotation flap.
8. The tensor fasciae lata (TFL) flap is the workhorse of
musculocutaneous flaps for coverage of trochanteric pressure
sores with or without a V-Y modification.
9. Wound dehiscence is a common complication in the surgical
treatment of pressure sores, and may be potentiated by
uncontrolled muscle spasms. Infection, poorly controlled
diabetes mellitus, malnutrition, and other factors that impair
wound healing can contribute.
10. The most important aspect of pressure sore postoperative care
is the relief of pressure, shearing, and tension on the newly
inset flap.
INTRODUCTION
Surgical treatment of pressure sores is common in the practice of
plastic surgery. Pressure sores develop in a variety of locations and for
various reasons. Generally, they are acquired in either the sitting or
lying position. The term decubitus ulcer should be avoided because it
misleadingly implies that the lesion was acquired while the patient
maintained a recumbent position, which is not always the case. When
describing lesions acquired due to pressure necrosis against a bony
prominence, the terms pressure sore or pressure ulcer are more appro-
priate and accurate.
The population at highest risk for developing pressure sores includes
patients with spinal cord injury, particularly those with acute trauma-
induced spinal cord injury. According to the National Spinal Cord
Injury Statistical Center, in the US in 2005, the estimated incidence
of spinal cord injury was approximately 40 cases/million population.
The prevalence in the US in July 2005 of spinal cord injury was esti-
mated at approximately 250 000.1 Critically ill patients, patients in
intensive care units, nursing home residents, and patients confined to
a bed or with decreased mobility are also susceptible to developing
pressure sores.
Besides the physical and emotional constraints incurred by the
patient with a pressure sore, the economic burden of the pressure sore
itself cannot be ignored when considering the natural history of the
lesion. Pressure sore patients require extensive support staff and pro-
longed hospitalization.
Pressure sores can be costly to the physician, the patient, and the
health care economy as a whole. Brem found that on average, patients
were charged $225 615 for the cost of care for pressure sores that they
developed while hospitalized.2
Pathophysiology
Many factors contribute to the development of pressure sores, but
the common denominators are pressure and necrosis.3 Other factors
include shearing forces, friction, moisture, decreased mobility,
decreased sensation, and spasticity (Table 17.1).
Pressure is measured as force per unit of area. The greatest areas
of pressure are found over bony prominences. In the prone position,
the knees and chest are the areas where the highest pressures can be
found; the buttocks and the heels bear the burden of pressure in the
supine position.
Patients who have spinal cord injury or patients who are bedridden
and confined to the supine position are also at an increased risk for
developing pressure sores over the occiput, sacrum, and heels. For
patients confined to a wheelchair or who spend most of their time in
a sitting position, the ischial tuberosities are at greatest risk.4,5
If external pressure is applied to the skin that is greater than the
end capillary bed pressure of 32 mmHg for a given region, tissue perfu-
sion to this area will be compromised and ischemia will ensue. For
example, in the sitting position, pressure over the ischial tuberosities 18
2 Table 17.1 Pathophysiologic factors that contribute to the
formation of pressure sores
Inverse time/pressure curve

No ulceration Ulceration
Factor Definition
600
Pressure Measure of force per unit of area 550
Shearing Deformation of a surface or tissue caused by forces 500
that tend to produce an opposite but parallel sliding 450

Pressure applied in mmHg

motion within the same plane
400
Friction Force that resists the motion of two bodies in contact 350
Moisture Progenitor of skin maceration 300

Decreased Synergistic factor along with pressure in the cause of 250

mobility pressure sore development 200
Decreased Loss of protective sensation may occur from 150
sensation neurologic damage or from various medications that 100
block pain receptors
50
Spasticity Supraspinal inhibitory pathways are interrupted 0 1 2 3 4 5 6 7 8 9 10 11 12
leading to spasticity
Time in hours

Fig. 17.2 Inverse time/pressure curve. (Redrawn from Husain T. An

experimental study of some pressure effects on tissues, with
reference to the bed-sore problem. J Pathol Bacteriol 1953; 66:347.)
Pressures over ischial tuberosities

10 shearing can occur in an immobilized patient when the head of the

20
80 40
60
80
100
Fig. 17.1 Pressures in mmHg over the ischial tuberosities in a
patient sitting with the feet supported. (From Whitney J, Phillips L,
Aslam R, et al. Guidelines for the treatment of pressure ulcers.
Wound Repair Regen. 2006;14(6):663-679.)
can be as much as 75 mmHg (Fig. 17.1). Dinsdale showed that a
constant pressure of 70 mmHg applied for 2 hours produces irrevers-
ible ischemia and tissue loss.6 However, not all tissues react to pressure
equally (Fig. 17.2). Muscle is the most sensitive tissue to ischemia
when compared to skin and subcutaneous tissue.
If early signs of ischemia such as erythema or skin changes are
seen, damage to the underlying muscle must be suspected. Necrosis
of the muscle may occur even before the overlying skin reveals signs
of its pending demise. Pressure may not always produce immediate
tissue necrosis. Decreased perfusion to tissues for a transient amount
of time can lead to reperfusion injury and make an area more suscep-
tible to other mechanical forces that contribute to pressure sore forma-
tion, such as shearing.
Another important physical force in the development of pressure
sores is shearing – a deformation of a surface or tissue caused by forces
84 that produce an opposite but parallel sliding motion. For instance,
bed is raised and the upper body slides down.
Friction is a force that resists the motion of two bodies in contact.
Friction can lead to small abrasions in the epidermis or when com-
bined with other mechanical forces can lead to destruction of the entire
epidermal–dermal complex. For example, when a patient is dragged
across the bed for repositioning or changing of the sheets on their bed,
friction occurs. Histologically, friction results in the removal of the
stratum corneum. This adds to the insult of the epidermis and pre-
disposes the patient to further skin breakdown and development of
a pressure sore.
Moisture is the progenitor of skin maceration, which when com-
bined with the forces described above, increases the risk of breakdown
and pressure sore development. It cannot be overemphasized that the
skin must be kept dry and clean. Bladder and fecal incontinence are
major sources of moisture in the immobilized patient that can lead to
accelerated pressure sore development. Bowel incontinence contributes
not only to maceration, but can cause bacterial invasion of pressure
sores. Combining a moist and warm environment from urinary incon-
tinence with the associated bacteria from bowel incontinence can
lead to a pressure sore that is grossly contaminated and infected. This
scenario may lead to further tissue loss due to infection or a more
serious complication such as sepsis.
Decreased mobility is a synergistic factor in the cause of pressure
sore development. Whether a patient is completely paralyzed or has
limited mobility, the ability to change body position plays a key role
in preventing pressure sores. Body position must be changed every 2
hours to prevent pressure damage to soft tissue.
Decreased sensation in any patient population is a risk factor for
the development of pressure sores. Loss of protective sensation may
result from neurologic damage or from medications that block pain
receptors. Patients who do not respond to painful stimuli have no
motive or incentive to change position to relieve pressure.
Paraplegic patients who are at the highest risk of developing pres-
sure sores may also suffer from muscle spasms, which can increase
the likelihood of developing a pressure sore. In these patients, the
supraspinal inhibitory pathways have been interrupted and cause not
only spasticity but also contractures. Muscle spasms must be treated
early with either pharmacologic or surgical intervention. Most
 Table 17.2 Pressure sore stages
Stage I Stage II
Depth Epidermis Into the dermis
Clinical signs Nonblanchable erythema Necrotic tissue
commonly, baclofen is used to control muscle spasms. Diazepam and
dantrolene have also been used7,8 Patients in whom pharmacologic
treatment of spasticity fails are candidates for more aggressive inter-
ventions such as neurosurgical ablation, amputation, and contracture
release.9
Classification
The most widely accepted classification system for pressure sores was
first described by Shea.10 In his system, he classified pressure sores by
their corresponding tissue depth and the pathophysiologic changes in
the tissue (Table 17.2). Over the years, adjustments have been made
to this classification, however it remains the standard for classifying
pressure sores.
Stage I pressure sores are limited to the epidermis. They are usually
first seen as an area of persistent nonblanchable erythema and acute
inflammatory response, including edema. Once the pressure is relieved,
the area of a stage I pressure sore may remain pink or red. With early
intervention, stage I pressure sores can be reversed simply by eliminat-
ing the pressure causing the sore.
Stage II pressure sores involve a partial-thickness skin loss. They
continue through the epidermis and into the dermis, and may present
as a deep abrasion, skin that appears cracked, blistered skin, or as a
shallow crater. There may be necrotic tissue and drainage. With proper
wound care and elimination of the contributing pathophysiologic
factors, stage II pressure sores can be treated and healed without
surgical intervention.
Stage III pressure sores involve full-thickness skin loss that extends
through the subcutaneous fat and down to, but not through, the deep
fascia. They may initially present as a deep crater. Thrombosis of small
vessels leads to fat necrosis, undermining, and tunneling; this is often
underestimated by the clinician. The inflammatory reaction in the
skin causes the epidermis to thicken and roll over the edge of the
wound leading to a distinct wound margin.
Stage IV pressure sores involve full-thickness skin loss with damage
to the deep fascia, muscle, and bony structures. There is usually exten-
sive undermining and necrosis of all tissue layers. Bone involvement
may include the possibility of osteomyelitis. These extensive pressure
sores may also involve joints causing destruction of joint capsules.11
INDICATIONS
Surgical reconstruction
● High-grade pressure sores (stage III and IV)
Contraindications
● Terminally or critically ill patient unable to tolerate general
anesthesia
● Sepsis
● Wound bacterial load greater than 105 CFU/g of tissue or the
presence of β-hemolytic streptococci
● Albumin less than 2.0 g/mL
17
Stage III Stage IV
Through the subcutaneous Full thickness skin loss with
fat down to the deep fascia damage to the deep fascia,
muscle, and bony structures
Fat necrosis, undermining, Extensive undermining and
and tunneling necrosis of all layers of tissue
● Preoperative vital capacity of less than 1500 mL due to prone
position required postoperatively
● Failure to appreciate and control spasticity
● Noncompliance with previous rehabilitation programs for
reconstruction of pressure sores and a history of recidivism
● Insufficient support systems for care after discharge
PREOPERATIVE CONSIDERATIONS
A complete history is required. It is important to thoroughly investi-
gate the medical cause and comorbidities that led to the development
of the pressure sore. The physical and mental health of the patient
should be evaluated. Psychiatric disorders may impede patient compli-
ance. Patients may need to tolerate prolonged postoperative position-
ing to achieve wound closure. Ask the patient about their social
circumstances and identify support systems. Discuss postoperative
needs, pressure-reducing devices for the bed and wheelchair, and
resources available. Also ask about illicit drug use and tobacco use. A
history of addictive drug use may prevent postoperative compliance,
and tobacco use can cause vasospasm, leading to wound dehis-
cence and flap failure. Medical records about any previous surgical
attempts at closure must be obtained prior to proceeding with surgical
intervention.
Special attention should be given to current control of spasticity
and thoroughly investigated prior to any intervention.
A complete review of systems is required, paying special attention
to activity level, symptoms of infection, nutritional deficiencies, and
bowel and bladder habits. Nutritional status and any recent weight
change is important, especially in the elderly and critically ill patients.
Bowel and bladder habits are also important, especially if the patient
has a colostomy or an indwelling catheter. Sterilization of the urinary
tract is optimal prior to undergoing surgical intervention for recon-
struction of a pressure sore.
A complete physical and neurological exam is performed. The pres-
sure sore is described in detail documenting its location based on
the underlying skeletal landmark and dimensional measurements,
including length, width, and depth. Manual palpation is required
to determine not only the depth of the pressure sore, but the possibil-
ity of extension to nearby structures. Signs of infection such as
erythema, exudate, odor, and necrotic tissue are detailed. Photog-
raphy with a ruler in the image is invaluable. Separate photographs
should be taken of the pressure sore up close and with anatomic
landmarks.
Nonoperative care
Prevention
An assessment tool such as the Braden Scale can be used to determine
those patients who are at risk for developing pressure sores. Patients
are evaluated for sensory perception, moisture, activity, mobility,
nutrition, friction, and shear. The score is inversely proportional to
the risk of pressure sore development.12 Reliance on an assessment 18
2 tool for prevention of pressure sores is inadequate, and clinical judg-
ment should always be included in the evaluation of a patient. A
physician or a nurse caring for the patient should do a daily examina-
tion of areas prone to pressure sores. Once identified, immediate
activation of treatment will decrease the likelihood of progression and
associated complications13 (Figs 17.3 and 17.4).
Wound debridement, cleansing, and wound
bed preparation
When considering the treatment of a pressure sore, the patient’s
comorbidities, and prognosis must be taken into consideration. In
terminally ill patients and those with multisystem organ failure, an
aggressive plan of debridement and cleansing may not be advisable.

Pressure ulcer protocol

Pressure ulcer

Primary care MD Wound care provider A pressure ulcer ("bedsore") is an injury caused
by constant pressure to the skin and muscle.
Severity ranges from mild (slight change in skin
Communication color) to deep (down to muscle and bone). When
a person cannot change position, pressure closes
tiny blood vessels that nourish the skin and supply
Medical record oxygen. When skin lacks nutrients and oxygen for
too long, the tissue dies and a pressure ulcer forms.

Initial visit

Topical Laboratory Digital photography, Physical Pressure

MRI
therapy tests objective measurement exam relief

CBC with Manual Diff Cellulitis or Based on: If osteomyelitis

Platelets Drainage or (1) ↓pressure is suspected
Hemoglobin A1C >2 months' duration (2) ↑blood flow
ESR Graph wound area length (3) Maximum
20
PT/PTT comfort
LFT's 15
Albumin 10
Prealbumin
5
Na+ Cl- BUN
Glucose 0
K+ CO2 Creatinine 2/21 3/21 4/21 5/21 6/21

Debridement

Repeat
debridement
Pathology Deep culture
until culture
is –
Evaluate for:
(1) Tumor + –
(2) Infection
(3) Necrosis
(4) Scar

Consider antibiotics, but

debridement is preferred

Minimal/decreased drainage
No cellulitis

Moist wound

For 2 weeks

<25% i per month

Plastic

Skin graft
Flap

Fig. 17.3 Pressure ulcer protocol (Redrawn from Brem H, Courtney L. Protocol for the successful treatment of pressure ulcers. Am J Surg
86 2004; 188:9S.)
 Algorithm for pressure relief surfaces
Patient at risk for
developing a pressure sore
Yes
Pressure-reducing surfaces are required
Static support surfaces may Dynamic support surfaces are
be used in patients who can required for patients who cannot
tolerate a variety of positions tolerate a variety of positions
Stage 3 or Stage 4 pressure
sores or multiple pressure sores
involving several turning surfaces
Low-air-Ioss or air-fluidized
beds are indicated
Fig. 17.4 Algorithm for pressure relief surfaces.
For patients who are stable, the goal of debridement and cleansing
should be to remove necrotic tissue, decrease bacterial count, and
produce a pressure sore with a granulated tissue bed. There should be
no local cellulitis, odor, or purulent drainage. If there is infection, a
topical antimicrobial can be combined with dressing changes to help
decrease the bacterial load. These include Dakin’s solution, silver-
containing compounds and antibiotic ointments. However, debride-
ment and irrigation provide the most rapid means of cleansing and
wound-bed preparation.
Debridement not only provides a means of preparing a healthy
wound bed, but also promotes wound healing. Wound-bed preparation
converts the chronic pressure sore into an acute wound with a more
favorable wound healing environment. All nonviable tissue, nonviable
scar, and infected tissue are removed by sharp, enzymatic, or mechan-
ical debridement. Solutions containing antiseptic agents are avoided.
Excision with a scalpel or scissors is the most effective method, and
in most cases minor excision can be done at the bedside. More exten-
sive debridement and hemostasis should be performed in the operating
room. Surgical debridement is contraindicated when vascular supply
is inadequate to support wound healing or in the absence of appro-
priate antibacterial coverage in the septic patient.
Dressings
The main objective in placing a dressing on a pressure sore is
to maintain a moist wound healing environment to facilitate re-
epithelialization and prevent desiccation.14 It is essential to protect
the surrounding skin to prevent propagation of the pressure sore or
development of new pressure sores. A large amount of exudate from
the pressure sore suggests the presence of infection, which should be
treated.
Negative pressure dressings can be used for grade III and IV pres-
sure sores that fail conventional nonsurgical therapy. Such therapy
removes exudates and debris while helping to increase wound perfu-
sion and formation of granulation tissue.15
Promotion of wound healing
Nutrition
All patients treated for pressure sores should have a nutritional assess-
ment, especially if surgical intervention is being considered. Malnutri-
tion may not only predispose a patient to developing a pressure sore,
but it is detrimental to the healing of pressure sores.16 Impaired ability
to feed oneself, recent weight loss, and decreased dietary protein must
be investigated and addressed. Pressure sores themselves can be a
17
source for loss of fluid and protein.10
Blood analysis is used to evaluate and follow the progression of
malnutrition. Albumin, prealbumin, and retinol binding protein are
indicators of malnutrition and can be objectively evaluated to help
determine the patient’s nutritional status. An albumin level greater
than 3.5 is optimal and has been shown to be a predictor in optimiz-
ing wound healing and preventing dehiscence.17 Patients who are
deemed to be at an increased risk of developing a pressure sore should
have their dietary supplementation to optimize intake and help prevent
pressure sore development.
All patients should have an adequate level of hydration. Dehydra-
tion increases sympathetic tone and decreases tissue perfusion.
Whether enteral or parenteral supplementation is provided, any
deficiency in vitamins, minerals, and trace elements need to be replaced
for proper wound healing.18
Positioning, pressure relief, and mechanical devices
Good nursing care is the cornerstone of pressure sore prevention and
detection. The patient should be positioned in bed at the lowest
possible degree of elevation that can be medically tolerated to prevent
shearing. The at-risk patient should be rotated from side to side every
2 hours being careful not to cause mechanical damage with the rota-
tion.19 Patients who are able to sit are instructed to avoid sitting for a
prolonged period of time and should relieve pressure at least every hour
and shift their weight every 15 minutes if possible. Seat cushions can
be used on a patient-by-patient basis, and ring cushions are avoided.
The objective, whether the patient is lying or sitting, is to avoid posi-
tions that compress soft tissue against bony surfaces. For patients with
existing pressure sores, it is important to avoid positioning that places
pressure on the existing pressure sore. Stewart described the technique
of bridging pillows as a means to accomplish pressure relief.20 This
method of pressure relief can be particularly helpful in bedridden and
critically ill patients.
Specialized beds such as low-air-loss or air-fluidized beds are helpful
in patients with advanced pressure sores such as stage III and IV pres-
sure sores and in patients who have multiple pressure sores that may
preclude them from pressure-relieving positions.21 Pressure sores can
still develop on these specialized beds, and they do not preclude
the need for strict nursing care and physician involvement in daily
surveillance
Transfusion
Patients with pressure sores may have a mild to moderate anemia
(hemoglobin 7–11 g/dL) and serum protein alterations similar to the
anemia of chronic disease (normocytic and normochromic with reduced
serum iron and transferrin with elevated ferritin).22 Erythropoietin
has been shown to be effective for the treatment of such anemia.23
Ultimately, the most effective and definitive treatment, however, is
closure of the wound.
Bacterial invasion (balance) and antibiotics in patients
with pressure sores
● Treat infections with appropriate antibiotics.
● Remove all necrotic or devitalized tissue.
● Perform a tissue biopsy and quantitative culture.
● If bacterial count is greater than or equal to 105 CFU/g of tissue or
if any tissue level of β-hemolytic streptococci is present, topical
antimicrobials are used to decrease the bacterial level.
● Discontinuation of topical antimicrobials once bacterial balance is
achieved minimizes possible cytotoxic effects.
● Exposed bone at the base of a pressure ulcer should be adequately
debrided and covered with a flap containing muscle or fascia. 18
2 A patient with a pressure sore may present with a distant infection.
Paraplegic patients are at risk for chronic urinary tract infections.
Quadriplegics have a higher risk for pneumonia.
A wound biopsy for quantitative tissue cultures is indicated for
pressure sores that fail to respond to treatment. Along with quantita-
tive cultures, Gram stains for qualitative bacteriology should also be
performed. Organisms are cultured to identify species and their cor-
responding sensitivities to both topical and systemic antimicrobials.
Staphylococcus aureus, Pseudomonas aeruginosa, Proteus mirabilis,
and Bacteroides fragilis are some of the more common bacteria found
in pressure sores. Systemic antibiotics typically do not reach therapeu-
tic levels in tissue. Qualitative studies are of importance because any
level of β-hemolytic streptococci can be detrimental to wound healing.
Topical antimicrobials are used for pressure sores with bacterial
counts greater than or equal to 106 CFU/g of soft tissue or any level
of β-hemolytic streptococci. Once bacterial balance is re-established,
discontinuation of topical antimicrobials is important to prevent any
detrimental effects and to prevent bacterial resistance.24 Bacterial
balance is ultimately controlled by irrigation, debridement, and closure
of the pressure sore.
Debridement of the infected bone is required to remove the loci of
infection followed by appropriate antibiotics administered for 3 weeks.
If clinical signs of sepsis persist in the patient or if the pressure sore
fails to contract, antibiotics are continued.
OPERATIVE APPROACH
Davis was the first person to suggest that pressure sores should be
treated with a tissue transfer, filling the defect and covering the bony
prominence.25 Since that time, the surgical treatment of pressure sores
has progressed to include a wide variety of surgical options including
musculocutaneous flaps. However, the concept of providing adequate
tissue to fill the defect and relieve pressure from the bony prominence
has not changed.
The surgical approach to pressure sores can be divided into two
general categories.
● The first category involves procedures that are required to promote
the healing process in a pressure sore that has failed less-invasive
management. This includes extensive debridement of wounds that
contain devitalized tissue, tunneling, and infection. Often topical
agents are not effective because of sinuses within the pressure sore
that cannot be manually palpated. The entire bursal sac of a pres-
sure sore must be removed along with any devitalized or infected
soft tissue or bone.26 Bacterial counts need to be less than 105
CFU/g of tissue, and there cannot be any b-hemolytic streptococci
in the wound for closure to be successful. Along with infected bone,
any bony prominence that could compress the soft tissue should be
removed, being careful not to damage surrounding structures.
● The second category for the surgical treatment of pressure sores
involves procedures designed for definitive closure. Pressure sores
should be surgically closed if there is no contraindication to under-
going the surgical procedure. Closure involves alleviating the pre-
viously discussed risk factors for pressure sores and filling the
defect with tissue to provide a tension-free closure. Flap coverage
should provide bulk to cover bony prominences. In designing the
flap, it is important not to compromise adjacent flap territories that
may be used in subsequent pressure sore closures. Suction catheters
are placed beneath the flap prior to closure to eliminate dead space.
The patient is positioned to minimize pressure on the suture line.
Guidelines for the surgical treatment of pressure sores are given in
Box 17.1.
Ischial pressure sore coverage
Ischial pressure sores are the most frequently encountered pressure
88 sores in paraplegic patients27 (Fig. 17.5A&B). Common flap closures
Box 17.1 Guidelines for the surgical treatment
of pressure sores (From Phillips L et al.
Evidence-based guidelines for the treatment of
patients with pressure ulcers. 2006;14:663–79)
● Unroof, explore, and treat appropriately any irregular wound
extensions, forming sinuses or cavities.
● Debride all necrotic and granulation tissue.
● Infected tissue must be treated by topical antimicrobials,
systemic antibiotics, or surgical debridement.
● Remove underlying bony prominences and fibrotic bursa cavities.
● Conservative bone excision is recommended.
● Fecal and urinary diversions are rarely needed.
● Consider radical procedures such as amputation or
hemicorporectomy only in rare and extreme cases.
● A pressure sore should be closed surgically if it does not
respond to wound care and there is not another
contraindication to the surgical procedure.
● Composite tissue closure leads to the best chance of sustained
wound closure.
● Management to address muscle spasm and fixed contractures
must occur preoperatively and continue at least until the
wound is completely healed.
for ischial pressure sores include the gluteus maximus in its entirety
or as an island flap, the inferior gluteal thigh flap (IGT), and the V-Y
hamstring flap.
Gluteus maximus flap
The inferior gluteus maximus island flap is an excellent first choice
because it provides adequate coverage of ischial pressure sores while
not compromising neighboring flaps for possible future use. The bulk
of the flap is provided by the gluteus maximus muscle (Fig. 17.6).
To fill the defect of the ischial pressure sore, the inferior gluteus
maximus musculocutaneous island flap uses a skin ellipse placed
above and lateral to the ischial pressure sore. The insertion of the
gluteus maximus muscle is released, and the inferior portion of the
muscle is separated from the superior portion. The sacral origin can
be left intact.28
An inferior gluteus maximus island flap provides adequate
coverage of ischial pressure sores while not compromising
neighboring flaps for future use.
When performing the ischiectomy, conservative debridement of
the ischial tuberosity is advocated. This helps not only to prevent
recurrence, but also to decrease occurrence of pressure sores in the
perineum and on the contralateral ischial tuberosity, which can occur
if radical ischiectomy is performed. The skin island should be larger
that the ischial pressure sore to provide tension-free closure and allow
placement of the suture line well away from the pressure sore. This
large skin island also allows for future advancement of the flap should
the pressure sore recur. Linear closure of the inferior gluteus maximus
island flap donor site makes this flap an ideal choice for ischial cover-
age. A variant reserved for nonambulatory patients includes inferior
rotation of the entire buttocks and gluteus maximus muscle.
IGT flap
The IGT can also be used for coverage of ischial pressure sores (Fig.
17.7). The IGT is a fasciocutaneous flap and unlike the inferior gluteus
 Gluteus maximus muscle
17
Hypogastric artery
Superior gluteal artery

Inferior gluteal artery

A
Fig. 17.6 Gluteus maximus muscle and its blood supply. The gluteus
maximus muscle derives its blood supply from the superior gluteal
artery and the inferior gluteal artery, both branches of the
hypogastric artery. The superior gluteal artery enters the gluteus
maximus just above the piriformis muscle and supplies blood to the
superior portion of the muscle. The inferior gluteal artery exits the
sciatic foramen and supplies blood to the inferior portion of the
muscle. (Redrawn from Mathes S, Nahai F. Clinical atlas of muscle
and musculocutaneous flaps. St Louis: CV Mosby; 1979:92–94.)

Inferior gluteal thigh flap

B
Fig. 17.5 Pressure sores. A, Stage III. B, Stage IV.

maximus island flap, lacks bulk because no muscle is included in the

flap design. The IGT is similar to the inferior gluteus maximus island flap
in that it does not compromise neighboring flaps for possible future use.

Operative technique
Dissection of the IGT flap is started distally and continued proximally
to the inferior border of the gluteus maximus muscle, taking care to
identify the posterior femoral cutaneous nerve. For complete mobiliza-
tion, the attachments to the iliotibial tract, intermuscular septum, and
femur must be released. Once mobilized, the flap can be rotated into
the ischial defect and closed without tension. Linear closure of the
donor site is attempted and augmented with skin grafts if necessary.

V-Y hamstring flap

Fig. 17.7 Inferior gluteal thigh flap. The flap is designed to be
The V-Y hamstring flap for ischial coverage is another option in the
approximately 32 cm in length and less than 10 cm in width
treatment of ischial pressure sores.29 It is based on the biceps femoris,
between the ischial tuberosity and the greater trochanter. (Redrawn
semimembranosus, and semitendinosus muscles and an overlying
from Hurwitz D, Swartz W, Mathes S. The gluteal thigh flap: a
triangular island of skin (Fig. 17.8).
reliable, sensate flap for the closure of buttock and perineal wounds.
Operative technique Plast Reconstr Surg 1981; 68:521.)
When using the V-Y advancement of the hamstring musculocutaneous
flap for coverage of ischial pressure sores, the patient must be placed
in the prone jack-knife position and fully flexed to maximize the 18
2 Muscles of the hamstring and their blood supply

Gluteus maximus

Profunda femoris
artery
Biceps femoris
Semitendinosus
Semimembranosus

Superficial femoral
artery

Fig. 17.8 Muscles of the hamstring and their blood supply. The three muscles of the hamstring originate from the ischial tuberosity except
for the short head of the biceps femoris, which originates from the linea aspera of the femur. The most lateral of the hamstring muscles is
the biceps femoris. It is the largest of the three hamstring muscles and can be found deep to the gluteus maximus and on top of the sciatic
nerve. The biceps femoris inserts onto the head of the fibula. Medial to the biceps femoris are the semitendinosus and the
semimembranosus, both of which insert onto the medial condyle of the tibia. The hamstring muscles derive their blood supply from
perforating branches of the profundus femoris, which pass through the adductor magnus to enter each of the muscles on their posterior
aspects. (Redrawn from Mathes S, Nahai F. Clinical atlas of muscle and musculocutaneous flaps. St Louis: CV Mosby; 1979:87–131.)

dimensions of the defect. The base of the flap should be the same width
as the defect of the ischial pressure sore. A V-shaped incision is made
from the medial and lateral borders of the defect distally. The biceps
femoris, semitendinosus, and semimembranosus are divided just distal
to the apex of the skin triangle.
Elevation of the musculocutaneous flap is started at the distal apex
and continued proximally along the deep surface of the muscles. The
origin of the short head of the biceps is divided at the linea aspera.
The proximal long head of the biceps femoris is freed from the gluteus
maximus, and the origins of all three hamstring muscles are detached
from the ischium. Failure to detach these muscles from the ischium
will hinder the flap’s ability to advance (Fig. 17.9A&B).
As with any other flap, pressure sores may recur with the V-Y ham-
string musculocutaneous flap. Recurrence of the pressure sore may be
more common with this flap because of placement of the suture line over
the area of the pressure sore and increased tension with hip flexion.30
The V-Y hamstring musculocutaneous flap can be readvanced mul- A B
tiple times to cover recurrent ischial pressure sores by enlarging it
and carrying the apex incision inferiorly to approximately 4 cm above Fig. 17.9 V-Y hamstring flap. A, The musculocutaneous flap is freely
the popliteal crease.31 The biceps femoris myocutaneous advancement mobile, attached only by its vascular pedicles. B, The flap is sutured
flap can be used in a similar fashion in patients who have motor func- into place to cover the ischial pressure sore defect making sure not to
tion in the lower extremities.32 Instead of elevating and advancing all place any sutures in the area of the previous pressure sore. The donor
hamstring muscles, only the long head of the biceps femoris is advanced site is closed primarily and all sutures are placed without tension.
for ischial pressure sore coverage. The short head of the biceps
femoris, semitendinosus, and semimembranosus muscles are left intact,
thus preserving flexion of the lower extremity. sore. Flap selection for the coverage of sacral pressure sores relies
heavily upon the gluteus maximus musculocutaneous flap. Options
include the V-Y gluteus maximus flap and buttocks rotation flap, which
Sacral pressure sore coverage can be re-advanced. This can be particularly favorable in patients who
Critically ill patients and anyone who is subjected to prolonged bed are ambulatory and who have developed a sacral pressure sore from
90 rest in the supine position are at risk for developing a sacral pressure prolonged bed rest.
Operative techniques
The inferior halves of the gluteus maximus muscles along with their
origins and insertions can be left intact when using bilateral superior
Partial use of the superior gluteus maximus muscle flap
17
halves of the muscles to cover sacral defects thus preserving hip
stability and ambulation potential.33
The gluteus maximus is a large muscle that provides adequate bulk
for reconstructing sacral pressure sores. All or a portion of the muscle
can be used depending on the ambulatory status of the patient and
based on either the superior or inferior gluteal artery (Fig. 17.10).
The patient is placed on the operating table in the prone position.
A large area of skin can be mobilized with the musculocutaneous flap
depending on the size of the sacral defect (Fig. 17.11A–E).

Trochanteric pressure sore coverage

The tensor fasciae lata (TFL) flap is the workhorse of musculocutane-
ous flaps for coverage of trochanteric pressure sores with or without
a V-Y modification.34 The TFL musculocutaneous flap allows for the
elevation of a large island of skin relative to the size of the muscle.
The lateral cutaneous branch of the 12th thoracic nerve and the
lateral cutaneous nerve of the thigh supply skin sensation to the
territory of the TFL, allowing transfer of sensate skin in paraplegics
with distal injuries (Fig. 17.12). Fig. 17.10 Partial use of the superior gluteus maximus muscle flap.
(Redrawn from Mathes S, Nahai F. Reconstructive surgery:
Operative technique
principles, anatomy, and technique. New York; Churchill
It is important that the patient is placed in the lateral decubitus posi- Livingstone; 1997.)
tion opposite to the side of the pressure sore when using the TFL flap
for coverage of a trochanteric pressure sore.

A B C

D E
Fig. 17.11 Surgical management of a stage III sacral pressure sore. A, Stage III sacral pressure sore. B, V-Y gluteus maximus flap.
Debridement, excision of the entire bursa, irrigation, and removal of any bony prominence is performed. A large area of skin can be
mobilized with the musculocutaneous flap depending on the size of the sacral defect. The superior and inferior aspects of the muscle are
elevated followed by blunt dissection to elevate the muscle from the underlying gluteus medius muscle. The insertion of the muscle is
released and elevated medially. The piriformis muscle is identified and aids in the identification of the superior and inferior gluteal arteries
anterior to the muscle approximately 5 cm from the sacral edge. C, The musculocutaneous flap is then transferred to the sacral defect.
D, The musculocutaneous flap is sutured into place with underlying suction catheter drains. The donor site is closed primarily.
E, Postoperative results. 19
2 Tensor fascia lata

Lateral cutaneous
branch of T12

Transverse branch of
lateral circumflex
femoral artery Lateral femoral
cutaneous nerve
Profunda femoris
artery

Tensor fascia lata

Sartorius
Gracilis
Rectus femoris
Vastus lateralis

Fig. 17.12 Tensor fasciae lata. The blood supply for the TFL flap arises from the lateral femoral circumflex artery, which is a branch of the
profunda femoris artery. Entrance of the lateral femoral circumflex artery into the TFL muscle can be found 10 cm below the anterior
superior iliac spine. This is an important landmark and should be noted prior to elevation of the flap. The lateral femoral circumflex artery
can have up to three branches, which divide the TFL into an upper, middle and lower third. The lateral cutaneous branch of the 12th
thoracic nerve and the lateral cutaneous nerve of the thigh supplies skin sensation to the territory of the TFL. (Redrawn from Mathes S,
Nahai F. Clinical atlas of muscle and musculocutaneous flaps. St Louis: CV Mosby; 1979:63–73.)

Elevation of the TFL begins distally at the apex of the flap design Tensor fascia lata
and progresses proximally (Fig. 17.13A–C). Occasionally a split-
thickness skin graft is required to assist in closure.35
This flap also serves as a secondary choice for coverage because
it can be re-advanced. The vastus lateralis muscle can be used as an
option for trochanteric coverage if the TFL has already been advanced
multiple times.

Optimizing outcomes
● Medically unstable patients are not candidates for pressure
sore reconstruction.
● Prior to flap coverage, the pressure sore must be adequately
A B C
debrided and bacterial counts must be less than 105 CFU/g of
tissue.
Fig. 17.13 Tensor fasciae lata flap. A, Trochanteric pressure sore.
● The presence of β-hemolytic streptococci is a contraindication B, The posterior portion of the V is drawn from the apex of the
to surgery. anterolaterally drawn line to the posterior perimeter of the
● Complete excision of the ulcer and its bursa as well as trochanteric pressure sore. The flap design must be large enough to
removal of any devitalized tissue is required. reach and cover the trochanteric defect. C, Final closure should be
● Infected bone and any bony prominence that could lead to tension free. (Redrawn from Siddiqui A, Wiedrich T, Victor L. Tensor
compression of the soft tissue is required must be removed. fasciae lata V-Y retroposition myocutaneous flap: clinical experience.
Ann Plast Surg 1993; 31:313.)
● The pressure sore defect must be closed with a healthy flap
that provides enough bulk to provide adequate padding over
the remaining bony structure.
● Closure must be tension free.
● Postoperative relief of pressure from the surgical site is
essential.
92

Fig. 17.14 Marjolin ulcer.
COMPLICATIONS
Reasons why musculocutaneous flaps fail to heal include infection,
spasticity, inadequate debridement, flap necrosis, and wound dehis-
cence. The size of the pressure sore defect after debridement has no
significant effect on the final outcome of closure, but comorbidities
that affect wound healing have a more detrimental affect.30 Postopera-
tive complications may lead to immediate or delayed recurrence of the
pressure sore.
Pressure sores tend to recur in patients with spinal cord injury.
Without sensation, these patients are unable to protect a musculo-
cutaneous flap from pressure necrosis.
Another unwanted complication is infection. The use of any post-
operative antibiotics must be based on wound cultures and sensitivities
to antibiotics determined by these cultures.36
Chronic wounds such as pressure sores have the potential for
malignant degeneration. Marjolin first described this process as a
tumor that developed in a chronic burn scar. The term Marjolin ulcer
is now used to indicate any malignant transformation that occurs in
a chronic wound (Fig. 17.14). Although the incidence of a Marjolin
ulcer in a pressure sore is rare (approximately 0.5%), a wound biopsy
is indicated for any pressure sore that clinically fails to respond to
treatment or develops an irregular, firm border to rule out underlying
malignancy.37 The well-differentiated squamous cell carcinoma that
develops is an aggressive lesion dictates a minimum of wide surgical
excision.
Wound dehiscence is a common complication in the surgical treat-
ment of pressure sores, and may be potentiated by uncontrolled muscle
spasms. Infection, poorly controlled diabetes mellitus, malnutrition,
and other factors that impair wound healing can contribute to wound
dehiscence. Paying attention to the basic principles of wound closure
is essential. Optimizing a patient’s preoperative comorbidities can help
avoid dehiscence after surgical closure.
POSTOPERATIVE CARE
It is imperative to optimize postoperative care for the success of the
procedure and to prevent postoperative recurrence.
The most important aspect of pressure sore postoperative care is
the relief of pressure, shearing, and tension on the newly inset flap.
Transfers and positioning require minimal pressure on the flap and
minimal tension on the suture line. Urinary catheterization is used to
prevent the patient from turning side to side for either micturition or
intermittent catheterization. Fecal diversion is usually unnecessary,
but a bowel regimen is recommended, possibly including an inten-
tional constipation. During this time, it is important to continue
nutritional support as needed. The initial surgical dressing combined
with a nonpermeable dressing can be left in place for 3–5 days post-
operatively to help prevent fecal and urinary contamination if neces-
17
sary. The decision to remove surgical drains should be determined on
a patient-to-patient basis.
Postoperative control of spasticity cannot be overemphasized.
Muscle spasms can cause dehiscence of the flap, hematoma, or necro-
sis and flap loss. Failure to appreciate and control spasticity is a
contraindication to surgical intervention. The patient’s anti-spasticity
regimen must be continued postoperatively.
Pressure sores will recur if the pathophysiologic means by which
they evolved are not alleviated. Recurrence rates as high as 91% have
been reported in the literature.38 Contributing factors for recurrence
include age of the patient, level of activity, malnutrition, hypoalbu-
minemia, and anemia. Smoking has been shown to be an independent
risk factor for the recurrence of pressure sores.39
Physical therapy
Physical therapy is initiated perioperatively. Passive and active range-
of-motion exercises are started immediately in the unaffected limbs.
Strengthening and toning exercises are encouraged in the upper
extremities to maintain baseline strength and tone. Between the 3rd
and 4th week postoperatively, range-of-motion exercises are started as
well as re-education concerning the patient’s role and responsibility in
postoperative rehabilitation.
A sitting regimen can be started between 2 and 3 weeks post-
operatively. During the initiation of the sitting regimen, vigilance is
required on the part of the physician, rehabilitative services, and the
patient to avoid recurrence of pressure sores. Patients are allowed to
sit for gradually increasing periods of time, lifting themselves every
10 minutes to relieve pressure.
CONCLUSION
The best treatment of pressure sores is prevention. Once they occur,
the key component in the management of any pressure sore is the
relief of pressure and avoidance of other physical forces that contribute
to the persistence and progression of the lesion. Adherence to wound
management and dressing guidelines optimize wound healing outcomes
and wound closure. Patient education, skin care, and rehabilitation are
essential components in pressure sore management. Optimization of
nutrition, wound bacterial balance, spasticity, and comorbidities is
required for all patients suffering from a pressure sore.
When considering the surgical reconstruction for coverage of a
pressure sore, it is important to remember that pressure sores can
recur. Proper flap selection will allow successful coverage while
preserving the territories of neighboring flaps for future use.
Postoperative management is as important as the operative proce-
dure itself. Positioning, control of spasticity, optimization of nutrition,
bowel and bladder management, wound care, treatment of comorbidi-
ties, and rehabilitation are indispensable allies for a successful outcome
in pressure sore reconstruction.
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