CHAPTER 98 • PRESSURE SORES
KAREN L. POWERS AND LINDA G. PHILLIPS
INTRODUCTION
-----------------------------------
A pressure sore is localized soft-tissue injury resulting from
unrelieved pressure, usually over a bony prominence. Because
areas of tissue pressure depend on patient position, the term
• pressure sore" is preferred, rather than bedsore or decubitus ulcer. Relieving the preasure caused by patient positioning
is the key to prevention and healing. Factors contributing to
the development of pressure SOle$ include decreased mobility,
decreased llensation, spasticity, shearing forces, friction, and
moisture. With so many factors playing a part in pressure sore
development, prevention and treatment frequently require a
multidisciplinary approach, often with the plastic surgeon
consulted for reconstruction of the soft-tissue defect.
The most widely accepted preaaure sore staging system
was revised by the National Pressure Ulcer Advisory Panel
in 2007 to include the original four stages and an additional
two stages regarding deep tissue injury and unstageable pressure sores (Table 98.1). Stage I includes intact skm with nonblanching erythema, stage II includes partial-thiclcness loss of
dermis, stage m includes full-thickness tissue loss, and stage
IV includes exposed bone, tendon, or muscle.1 Additional classi.fication includes SJI$'f)ec;ted deep tissue in;ury, usually characterized by maroon localized intact skin or blood-filled blister,
and unstageable, which is a full-thickness ulcer with eschar
at the base. Limitations exist in this system; signs like skin
erythema can be present in more than one stage and dark skin
pigmentation can actually obscure the presence of erythema,
necessitating other diagnostic signs like increased skin temperature, edema, and induration, to accurately stage the wound.
Long-standing wounds of the pelvic girdle warrant careful
examination and possible imaging to evaluate for extension
into deeper structures, such as the acetabulofemoral joint.
EPIDEMIOLOGY
------------------
------------------
The incidence of pressure sore formation is variable but
the patient populations commonly studied include those in
acute care settings, nursing home patients, and paraplegic
NATIONAL PRESSURE ULCER ADVISORY PANEL
STAGING SYSTEM, 2007
• STAGE
• DESCRIPTION
Intact akin with non-blanchable rednen of a
localized area
D
Partial-thickness loss of dermis presenting as
a shallow open ulcer with a red pink wound
bed
m
Pull-thickness tissue loaa. Subcutaneous fat
may be visible but bone, tendoo, and muscle
are not exposed
IV
Full-thicknes~
tissue loss with exposed bone,
tendon, or muscle
-----------------
Data &om National Pressure Ul<:er Advbory Panel. NPUAP l'temlle
Ulcer StageS/Categories. bttp:llwww..npoap.org/mourca/educati~
and-cliDkal-mource.afnpuap-pressure-aker-stagetattegorieal
populations. In general, pressure sores develop in approximately 9% of all hospitalized patients, affecting 2.5 million
people annually.2 For acute and long-term cate facilities, the
overall reported prevalence ranges between 3.5% and 29.5%.'
In addition to causing pain, suffering, and disability, pressure
sores contribute to over 60,000 deaths per year according to
the N ational Pressure Ulcer Advisory Panel.1 Data from the
National Pressure Ulcer Long Term Care Study suggest that
up to 19% of new patients develop a pressure ulcer while
in long-term care and 22% arrive with an existing pressure
ulcer. 4 Beginning in October 2008, The Centers for Medicare
and Medicaid Services ended reimbursement of acute care
facilities for the development of a hospital-acquired stage m
or IV pressure sores, thereby compounding the challenge of
pressure sore prevention with the essential task of documentation of pressure sores present on admission.
Multiple studies have demonstrated that age, moisture,
immobility, and friction/shear are key risk factors.J Impaired
sensory perception is known to contribute to the development
of pressure sores but the incidence in patients with spinal cord
injuries varies greatly. The Braden Scale, incorporating factors
such as mobility, can be used to predict an individual's pressure sore risk. Stal et al.' cited a 20% incidence in paraplegic
patients and a 26% incidence in patients who were quadriplegic. For the majority of patients, wounds develop in either the
supine or seab:d position. Up to 75% of all pressure sores are
located around the pelvic girdle. This is not unex~d, as it
mirrors the distribution of pressure in supine and sitting positions (Figures 98.1 and 98.2). A study of a large cohort from a
statewide Arkansas registry cited significant risk factors in the
spinal cord-injured patient, including being underweight, use
of pain medications, smoking, suicidal behaviors, history of
incarceration, and alcohol and drug use. 7
PA1HOPHYSIOLOGY
--------------
Compression of soft tissues results in ischemia and, if n ot
relieved, it will progress to necrosis and ulceration, even in
well-vascularized areas (Figure 98.3). What is seen on the
surface is often merely the trp of the iceberg, as confirmed
by pressure measurements taken over bony prominences•
(Figure 98.4). In susceptible patients, progression from excessive pressure to irreversible ischemia and tissue necrosis is
accelerab:d by infection, inflammation, edema, and other factors that are not yet understood.
Pressure
----------
Ischemia occurs when external pressure exceeds the capillary
pressure, which was shown by Landis9·l0 in the 1930s to be 12
mm Hg on the venous end and 32 mm Hg on the arterial end.
I£ the extemal compressive lorce exceeds capillary bed pressure (32 mm Hg), atpilllll')' perfusion is impaired 11111d ischemia
will ensue. Original dog studies demonstrated an inverse parabolic relationship between the amount of pressure and duration of exposure (Figure 98.5). Early studies demonstrated
that pressure of 70 mm Hg applied over 2 hours was sufficient
to cause pathologic changes in dogs. Dinsdale11 confirmed
these results in a pis model; perhaps just as importantly, he
was also able to demonstrate the absence ol injury if pretsure
could be relieved for as little as 5 minute~, even with pressure~
as hish as 4SO mm liB- Similarly. Daniel et al.12 demonstrated
that pressure of 500 mm Hg applied for 2 hours, or pressure
989
990
Pan IX: Tl'Wik and Lower h:tremity
FIGURE 98.3. Unusual prenure tore of lateral thorax.
heels, buttock, and sacrum. ln the sitting position, pressures
were greatest near the ischial tuberosities.
Inflammation
FIGURE ~.1. Distribution of pressures in a normal man. A. Prone.
B. Sitting. (From Lindan 0, Greenway RM. Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and
sitting positions using a "bed of springs and nails." Arch Plrys Med
Rehabil. 1965;46:378.)
Maintenance of soft-tissue integrity requires tightly regulated
interactions between cells, growth factors, their receptors,
extracellular matrix molecules, and a variety of proteases and
their inhibitors. When tissue is injured by causes such as unrelieved pressure,. there is a demargination and influx of cells
responsible for inflarwnation. For injuries to heal, a series
of events unfolds, including vasoconstriction/vasodilatation,
c:oagulation, influx of proinflammatory cells like neutrophils
and macrophages, and, finally, matrix formation/maturation.
In chronic wounds, there is a breakdown in this sequence,
leading to a non-healing wound. Altered immune function
has been implicated in the development of pressure sores and
of 100 mm Hg for 10 hours, was sufficient to cause muscle
necrosis. Interestingly, it was not until pressure of 600 mm
Hg was applied for 11 hours that ulceration of the skin could
be seen. Not only did these results c:onfirm. the relationship
between pressure and time, but they also demonstrated that
the initial pathologic c:hanges occurred in the muscle overlying
the bone, followed by the more superficial soft tissue, involving the skin last.U Several classic st:lldies investigated pressure
and its effects as it relab:s to location, time, and intensity in
humans (Figures 98.1 and 98.2). ln the supine position, the
maximal recorded pressures were 40 to 60 mm Hg near the
Sitting, feet supported
Sitting, teet unsupported
FIGURE 98.2. Distribution of pressures in a normal man, sitting.
(From undan 0, Greenway RM. Piazza JM. Pressure distribution on
the surface of the human body. L Evaluation in lying and s.itting pos.itions using a ..bed of springs and nails.,. Arch Phys Med Rehabil.
1965;46:378.)
FIGURE 98.4. Cone-shaped pattern of injury rerulting from unrelieved pre55ure. The highest pressure and greatellt injury ill deep,
adjacent to the bone. The cutaneous wound ill only the "tip of the
iceberg..,.
Chapter 98: Pressure Sores
calories should be delivered daily.U Optimization of nutritional parameters must be balanced against practicality; some
patients will never achieve normal albumin levels until their
huge wounds are closed.
Ill 550
:z:
e soo
E •so
z
o
...
400
~
350
II:
300
•"'
I
Infection
.., 2SO
~
"'
100
~ 150
Ill
a.
991
100
5o()
0 ~~
2~
3~
4~
5~
6 ~~8~
9--10~~
11 ~12~
TIME IN HOURS
FIGUJlE ~8.5. Inverse relationship between time and pressure in the
formation o£ pl'CS&ure sores.
molecular evidence points to an imbalance between matrix
metalloproteases (MMPs) and tissue inhibitors of metalloproteases (TIMPs). MMPs, especially 1 and 9, are key to cell
signaling and migration, whereas TIMPs, especially 1 and 2,
bind to these proteases and presumably protect uninjured
tissues. Numerous subsequent studies have documented the
presence of elevated levels of various MMPs and decreased
levels of TIMPs in chronic wounds, or an imbalance between
the levels of MMPs and TIMPs.14 In patients with spinal cord
injuries, the loss of sympathetic tone results in vasodilatation
of denervated tissues, which further intensifies this problem.
Edema
Approximately 80% of soft tissue mass is fluid. External
pressure on soft tissue increases plasma extravasation, which
leads to edema formation, a significant factor in pressure sore
formation. Denervation contributes to pressure sore development through loss of blood vessel sympathetic tone and its
subsequent vasodilatation, vessel engorgement; and edema.
Circulatory deficiencies, such as heart failure, renal failure,
and venous insufficiency, are risk factors for pressure sore
formation in part due to their propensity to increase edema
in dependent soft tissue. On a molecular level, inflammatory
mediators such as prostaglandin Ez released in response to the
trauma of compression increase leakage through the cell membranes and increase interstitial fluid accumulation.
Compression of soft tissue impairs lymphatic drainage, leading to edema, ischemia, and other conditions favorable to
colonization and infection by microorganisms. It is known
that bacterial counts increase in compressed areas. Robson
and Krizek1' quantified the effect of pressure on bacterial
count, showing that incisions created in areas of applied pressure and inoculated with known concentrations of organisms
allowed for a 100-fold greater bacterial growth than in areas
not subjected to pressure. The proposed mecllanisms include
impaired immune function, ischemia, and impaired lymphatic
function. Both pulmonary and urinary sources cause seeding
and subsequent infection of pressure sores. Indwelling bladder
catheters or self-catheterization programs can result in urinary
sepsis in one-third of paraplegic patients. If left untreated, urinary .infections can be a constant source of bacteremia.
Pressure sores may or may not present with local infection
(deep or superficial). The removal o£ all nonviable tissue is the
essential first step. After a soft-tissue debridement; a specimen
should be sent to the microbiology laboratory to assess not
only the bacterial types and sensitivities but also for quantitative culture. A result of more than lOS organisms per gram
of tissue is diagnostic for invasive infection and is predictive
of failure of surgical closureP Swab cultures are generally
discouraged because they often represent only surface contaminants. Diagnosis of osteomyelitis depends on bone biopsy
to identify the causative organism and magnetic resonance
imaging to determine the extent of involvement. Surgical closure without eradication o£ bone infection through reseaion
of devitalized bone is associated with a high recurrmce rate.
Osteomyelitis from a pressure sore requires a surgical solution, not a medical solution.
Appropriate intravenous antibiotics for cellulitis or osteomyelitis, along with topical antimicrobials, such as silver sulfadiazine, mafenide acetate, and buffered Dakin's solution,
should be used as adjuncts to surgery in the process of clearing
infection. Although Dakin's solution diluted to 0.025% has
been shown to be bactericidal with preservation of fibroblasts,
all topicals should be used for a limited time after debridement
to avoid delayed wound healingP
PREOPERATIVE CARE
Relief of Pressure
As Tchanque-Fossuo et al.s noted in a 2011 review of evidence-based approaches to pressure sores, the goals of management for a patient with a pressure sore are (1) prevention
of complications, particularly invasive infection, related to
the existing sore; (2) preventing the existing sore from getting
larger; (3) preventing sores in other locations; and, if possible,
(4) closure of the wound. Most authors report high recurrence rates after surgical closure of pressure sores. Suc:.c:essful
pressure sore coverage is multifactorial but key components
include resolution of infection, the preoperative/postoperative
relief of pressure, and, for uses of <:hronically non-ambulatory patients, the control of spasm and c:ontrac:tures.
The relief of pressure both preoperatively and postoperatively
is the key to success, because healing will not occur in the presence of ischemia and/or neaosis. It is well known that relieving the pressure over a bony prominence for 5 minutes every
2 hours will allow adequate perfusion and prevent breakdown.11 Patient; family, and medical staff education is paramount in this goal, and it must be performed in both supine
and sitting positions. Adjuncts include dynamic and static
pressure-reducing support surfaces, such as foam, wheelchair
cushions, specialized mattresses, cushions, and mattress overlays. Surgical staff should use all available means, such as "heel
floating" and intermittent scalp massage by anesthesia staff, in
addition to pressure point relief to minimize development of
pressure sores during procedures in the operating room.
Nutrition
The nutritional condition of the patient must be evaluated.
Normal healing potential exists as long as serum albumin is
maintained above 2.0 gldL. In addition to an adequate supply of micronutrients such as zinc, calcium, iron, copper, and
vitamins A and C, a diet with sufficient protein is required
for optimal healing of pressure sores. The nutritional literature suggests a requirement of 1.5 to 3.0 glkgld of protein to
restore lost lean body mass, and 25 to 35 callkg of non-protein
Spasm
Spasticity is common in patients with spinal cord injuries and
is a key contributor in the development of pressure sores,
especially as it relates to shear. In their review of long-term
care patients in Germany, Lahmann et al.11 found that the
presence of friction and shear had the strongest association
with pressure sore formation. The incidence of pressure sores
992
Pan IX: Tl'Wik and Lower h:tremity
varies with the level of spinal cord injury. The more proximal the lesion, the higher the incidence of spasm: near 100%
in the cervical region, 75% in the thoracic region, and SO%
in the thoracolumbar region.U Treatment of muscle spasticity should be implemented prior to surgery. The most common medical treatments for muscle spasms include baclofen,
diazepam, and dantrolene. Botulinum toxin is an emerging
treatment for spasticity and has been shown to be effective
in reducing localized spasticity of the upper and lower limbs
with minimal adverse effects.111 The lasting effects of the botulinum toxin treatment for muscle spasticity are approximately
3 months. If patients fail to respond to medical therapy, surgical intervention may be required, including peripheral nerve
blocks, epidural stimulators, baclofen pumps, and rhizotomy.
Rhizotomy, the interruption of spinal roots within the spinal
canal, can be surgical or medical, the latter using subarachnoid blocks with phenol (phenol rhizotomy).
Contractures
Bedridden patients, especially those with long-standing denervation and!or altered sensorium, tend to develop joint contractures through tightening of both muscles and joint capsules.
Contractures are common in hip flexors and contribute to the
formation of trochanteric, knee, and ankle ulcers. Patients
with significant hip and/or knee contractures should have
every attempt made to tteat the contraaures prior to surgery
to help prevent rec:urrenc:e. If physical therapy is unsuccessful at relieving the contractures, tenotomies are performed. ln
mobile, wheelchair-bound patients, however, releasing the hip
contractures can lead to a flail extremity, which may interfere
with transfers. u
Comorbidities
Many chronic medical conditions-such as diabetes, smoking,
peripheral vascular disease, and cardiovascular disease-are
known to impair wound healing. In diabetics, glucose levels and hemoglobin Ale should be checked and optimized
because hyperglycemia slows wound healing and increases the
risk of wound dehiscence and infection. Recent work found
that hemoglobin Ale greater than 6% was associated with
both dehiscence and recurrence and that younger age and
hypoalbuminemia were associated with early flap failure.20
Anemia can be an indicator of poor nutrition or chronic blood
loss and should be worked up and corrected. In spinal cord
injury patients, management of fecal soilage of the wound is
necessary through alteration of the bowel routine or a diverting colostomy in selected patients.
SURGICAL TREATMENT PLANNING
When the challenges such as consistent pressure relief, adequate nutrition, eradication of infection, complete debridement, and reliable patient and family education have been
accomplished, consideration can be given to surgical closure.
Because the reaurence rate of pressure sores has been reported
to be as high as 91 %t the goal is to provide soft-tissue coverage of the pressure sore defea, while maintaining as many
options as possible for future use. A number of strategies for
closure have been attempted in the past and in general should
be avoided. The temptation to perform a primary closure
should be resisted even if the tissues seem to rex~ppro:ximate
easily. By definition, a pressure sore has an absolute tissue
deficiency, and simply pulling the tissue together over a bony
prominence will almost surely lead to tension and dehiscence.
Skin grafting bas been attempted with limited success because
of the lack of bulk and poor durability in the face of the pressure and shearing forces. lt is only successful in a patient
where acute illness and immobility will be resolved. More
successful strategies include the use of musculocutaneous and
fasciocutaneous flaps, with each having its advantages. Flaps
that include muscle have significant bulk and excellent blood
supply. They, therefore, can be useful where a significant softtissue defect is present and also where a history of infection is
a consideration. On the downside, muscle is not a good choice
in ambulatory patients, as sacrificing muscle may lead to functional impairments.
Even if the patient is ambulatory, surgical planning for
patients with pressure sores should include deep venous
thrombosis risk stratification and appropriate prophylaxis.
Non-ambulatory spinal cord injury patients have additional
anesthetic risks when compared with non-spinal cord injury
patients of a similar American Society of Anesthesiologists
class. Autonomic dysreflexia can produce bradycardia and
hypotension, or tachycardia and hypertension. This condition,
plus the hyperkalemia that can be caused by the use of succinylcholine in spinal cord injury patients, must be discussed
preoperatively with the anesthesia team.
For all patients in general and acute spinal cord injury
patients in particular, prevention of pressure sores acquired in
the operating room is paramount through intraoperative pressure relief, which can include such measures as "floating the
heels." Moving and positioning patients with pressure sores
also requires coordination of the surgical, anesthesia, and support staff. Usually patients are anesthetized on thcir stretchers
and transferred prone to the operating room bed. This process
reversed at the completion of the case as patients are often
positioned onto their freshly transferred tissue for extubation.
OPERATIVE MANAGEMENT
Debridement
Debridement of the pressure sore removes necrotic tissue,
decreases the bacterial count and bio.film, and converts a
chronic wound into an acute wound. The presence or absence
of sensation in the tissues affected by pressure ulceration
becomes an issue most often when sharp debridement is considered. The pain associated with the adequate removal of
necrotic tissue in sensate patients makes bedside debridement
impossible. ln insensate patients, bedside debridement can be
performed within reason, although the safety and extent is
more often related to the control of hemorrhage. At the start
of the debridement procedure, the cavity can be painted with
a dilute solution of methylene blue and hydrogen peroxide to
help define the cavity and leave a visual guide for excision.
After the removal of the necrotic tissue, specimens of viable tissue should be sent for quantitative culture to aid in postoperative systemic and topical antibiotic coverage. Postoperatively,
the wound is packed and dressings changed every 6 to 8 hours.
Ostectomy
Removal of the bony prominence is an integral but tricky part
of the surgical treatment of pressure sores. Radical ostectomy
should be avoided so as to prevent excessive bleeding, skeletal
instability, and redistribution of pressure points to adjacent
areas. Ischial ulcers best illustrate this as total ischiectomies
often result in the formation of a contralateral ischial ulcer.
Bilateral ischiectomy has also been proposed, but redistributed pressure has caused perineal ulceration and urethral
fistulas. Therefore, removing the minimum amount of bone
necessary when debriding ischial pressure ulcers is essential.U
Closure
When planning a surgical strategy, the surgeon should consider
not only the present surgery but also the need for subsequent
surgical procedures. The choice of closure strategy depends not
only on the location, size, and depth of the ulcer but also on
the previous surgeries performed. Primary closure, although
tempting, is avoided. These wounds represent an absence of
tissue and primary closure leads to tension, a scar over the
Chapter 98: Pressure Sores
original bony prominence, and dehiscence. Skin grafting has
a low success rate, as grafting ~nds to provide unstable coverage. Musculocutaneous flaps provide blood supply and
bulky padding and are effective in treating infected wounds.
Disadvantages include sensitivity to external pressure, functional deformity in ambulatory patients, and lack of bulk in
the elderly and in spinal cord patients. Fasciocutaneous flaps
offer an adequate blood supply, durable coverage, and minimal potential for a functional deformity, and they more closely
reconstruct the normal anatomic arrangement over bony
prominences. The disadvantages include limited bulk for the
treatment of large ulcers. In a recent reriew of .94 patients with
saaal and ischial pressure wounds, there was no statistical di£ference in recurrence, complications, or morbidity between closure wish fasciocutaneous flap and with myoc:utaneous !aps.:u
Ischial Defects
Ischial pressure sores develop in patients who are seated, often
in wheelchairs, for long periods of time. Because patients
almost always return to sitting after repair of their ischial
pressure sores, the recurrence ra~ traditionally has been high;
Conway and Griffith reported a recurrence rate of 75% to
77%. R.e«nt work cites recurrence rates as low as 19% to
33% that may be due in part to improved wheelchair cushions
and other modalities.:U Ischial wound location, however, continues to correlate with late recw:rence.20
Closure of an ischial defect is most commonly achieved
with fasciocutaneous flaps or myocutaneous flaps. Perforator
and free-flap reconstruction have been described but currently is not a mainstay of ischial pressure sore treatment.
Some of the more commonly used closure strategies are featured in Figure 98.6. Given the high recurrence rate of pressure wounds. flap design should allow coverage of the ulcer
but should not prevent the use of other flaps in the future.
Important considerations for flap design include size and
depth of the ulcer, quality and pliability of the surrounding
skin, presence of previous surgical scars, and the ambulatory
status of the patient. For example. the inferior gluteal musculocutaneous flap, based on the inferior gluteal artery, uses
only the lower half of the gluteus maxi.mus muscle. This rotation flap does not preclude later use of the posterior thigh flap
and is less debilitating in ambulatory patients.
In the superiorly based gluteal flap (Figure 98.7), care
is taken to avoid incisions over bony prominences when
the patient is in the seated position. The biceps femoris,
Medially based tb igh flap
V-Y Hamstring advancemem flap
Glu teal island th igh flap
Tensor fascia
lata flap
FIGURE 98.6. Flaps for clofW'e of iKhia1 wounds.
993
GraciJis
flap
994
Pan IX: Tl'Wik and Lower h:tremity
FIGURE 98.7. Flaps for closure of sacral wounds.
semimembranosus, and semitendinosus musculocutaneous
flaps are said to be effi:ctive for ischial ulcers and they can be
re-advanced. They are most reliably designed as a V-Y pattern,
but do have several disadvantages, including closure is always
under tl:nsion, the scar is directly over the maximal pressure
point, and hip flexion tends to cause dehiscence. The tensor
fascia lata (TFL) flap can occasionally be used to close ischial
ulcers, although the distal aspect of the TFL flap is usually too
thin to offer adequatl: padding, making the TFL flap, in general, not the best choice. For more complex, deeper, or larger
wounds, a combination of flaps may need to be employed.
Sacral Defects
Sacral pressure sores occur in patients in the supine position,
most of whom have had an acute illness. Musculocutaneous
or fasciocutaneous flaps are the mainstays of surgical therapy but the use of perforator and free-flap reconstrllction is
increasing (Figure 98.7). Some groups have published that
their first choice for reconstruction of ischial and sacral pressure sores is free tissue transfer with microvascular anasto·
mosis to the gluteal vessds.23 Other surgeons using pedicled
tissue transfer cite a 21% total recutTence rate after coverage
with any flap of sacral wounds, with a lower (17%) recurrence rate after reconstruction with fasciocutaneous flap. 24
The most commonly described musculocutaneous flaps are
based on the gluteus maximus muscle. The gluteal flap can
be based superiorly or inferiorly, part or all of the muscle or
both muscles may be used; it can be constrllcted of muscle or
muscle and skin; and it may be rotated, advanced, or turned
over (Figure 98.8). Other flaps available include the transverse
and vertical lumbosacral flaps, based on lumbar-perforating
FIGURE ~8.8. Glutl:al flap to saaal prc:Mure sore. A. Sacral wound. B. Oosure with gluteal fascioc:utaDeOus flap.
Chapter 98: Pressure Sores
FIGUJlE 98.9.
995
Ten&Or fascia lata flap to ischial pressure sore. A. Flap design. B. Flap closure.
vessels, although these have significandy less bulk and, consequendy, are less useful in deeper wounds.
Trochanteric Defects
Trochanteric ulcers develop in patients who lie in the lateral
position, especially in those who have significant hip flexion
contractures. Perforator flap reconstruction of trochanteric
pressure wounds is possible with a pedicled anterolateral thigh
flap. However, the most commonly used flap for treatment of
this location is the TFL flap. This highly reliable flap is based
on the perforating vessels from the TFL muscle, although caution is advised as the distal aspect of the flap has a random
blood supply that sometimes necessitates a delay procedure.
Sensation from the nerve roots ofLl, 1.2, and L3 by the lateral
femoral cutaneous nerve makes this a potentially sensate flap
in patients with spinal cord injury below L3. Rotation of the
TFL flap results in a T·shaped junction between the flap and
a primary dosed donor site that is prone to dehiscence, often
the donor site is skin~ to avoid dehiscence (Figure 98.9).
Other Considerations
Only the most common pressure sores have been discussed
in this chapter; however, if an anatomical location can serve
as a pressure point, then it has the potential to develop a
wound when subjected to unrelieved pressure (Figures 98.1
and .98.2}. Some less common pressure sores, like those at
the ear or scapula, ofb:n can be dosed primarily or with local
tissue rearrangement. Other pressure sores, such as those at
the heels, are difficult to treat (Figure 98.10). In patients who
have multiple pressure sores or who have undergone multi·
ple previous procedures, there may not be any local options
remaining. In extreme cases of pelvic girdle or lower extremity
pressure sores, it may be necessary to consider total thigh flaps
in which the femur is removed and the thigh tissue is used to
close the wound (Figure 98.11).
POSTOPERATIVE CARE
Many of the preoperative care considerations (e.g., nutrition
and management of chronic conditions such as spasm and diabetes} continue into the postoperative period. Careful nursing
care is critical to postoperative success. An absorptive nonocclusive dressing is used in an effort to avoid macerating the
wound. The control of urine and stool is important and in
some cases colostomies are required pre-operatively. Drains
are placed intraoperatively to remove serous fluid and to aid
in apposition of the flaps to the wound bed. Because of probable intraoperative bacteremia, broad-spectrum antibiotic
therapy is continued during the perioperative period. The
antibiotics are modified to fit the sensitivity results of intraoperative cultures as these results become available. Pressure
relief for the surgical site, usually involving bed rest and a
pressure-relief bed, is of utmost importance. The patients are
positioned to avoid pressure on the operative site, with turning every 2 hours, and use of low-air-loss mattresses when
available. Patients are kept in the postoperative position,
with no pressure allowed on the surgical site for 2 to 3 wedts.
Before reseating after ischial pressure wound coverage, the
patient's wheelchair should be evaluated to ensure a proper
fit and pressure distribution. There is no consensus on reseating protocols, but it is agreed that reseating must be gradual.
A common protocol starts with 30 minutes the first day and
then adds a 0.5-hour increment daily if tolerated without
compromise of the surgical site.1
CO?viPLICATIONS
In addition to the acute complications related to treating pres·
sure sores-hemorrhage, pulmonary and cardiac complications, and infection-a few long-term complications warrant
discussion.
Recurrence
The reasons for high rates of recurrence are multifactorial.
The underlying medical problems that contributed to ulcer
996
Pan IX: Tl'Wik and Lower h:tremity
D
FIGURE ~8.11. Total thigh flap. A. Large recurrent ischial wound.
B. The distal lower extremity was amputated and the femur was
removed with the specimen. C. The thigh tissue provides abundant
tissue that can be folded over the wound. D. Closed wound.
c
formation stiU exist. The presence of spinal cord injury and/
or altered mentation in the elderly persist. The labor-intensive
nursing care issues (turning, local wound care, and avoidance
of urine and fecal contamination) may not have changed from
the preoperative setting. Social issues like the lack of financial resources, inadequate family and/or community support,
and the use of drugs and alcohol may also be present. Many
studies observed that the first 15 to 22 months are the most
vulnerable time period for recurrence. A recent review by Keys
et al.20 found a 39% recurrence rate of pressure sores after
flap closure, with poor blood glucose control, younger age,
and poor nutritional status (hypoalbuminemia) as significant
risk factors. Patients with multiple risk factors had operative
success rates that approached zero.
Carcinoma
In 1828, Jean Nicholas Marjolin described a tumor that was
present in a chronic wound. The term MarjoUn ulcer is used
to describe carcinoma arising in a ~hroni~ wound. The most
~on cell type is squamous ceU carcinoma. In contrast to
most other tumors of this type, these tumors tend to be aggressive with 2-year survival rates varying from 66% to 80%.
Their metastatic rate, as compared with that of Marjolin
ulcers arising in bum scars, is significandy higher at 61% versus 34%. The time interval of development is also reduced.
The usual time to appearance is 25 years when compared with
more than 30 years in bum-related carcinomas, but it can be
as short as 2 years. Because of the aggressive nature of the disease, wide surgical excision to clear margins is recommended.
Prophylactic lymph node dissection is not recommended, but
therapeutic node dissection is indicated in the case of clinically
involved nodes. Adjuvant radiation and/or chemotherapy may
be indicated in cases of unresectable tumors or if the patient
refuses surgery.
Nonsurgical Treatment
The ultimate treatment of pressure ulcers is not necessarily
a surgical correction. If proper preoperative assessment and
Chapter 98: Pressure Sores
preparation are performed, there will usually be a period of
time in which the ulcers can be observed. If during this time
period the ulcer appears to be healing significantly, continuation of nonoperative treatment is indicated. Some patients
may never be candidates for surgical correaion because of
significant medical problems. In these cases, avoidance of
unrelieved pressure. control of infection (local and remote),
control of incontinence, and improved nutrition may lead to
successful ulcer closure, or at least may allow for a stable
wound that does not progress.
Debridement of devitalized tissue and wound care remain
the foundation of pressure sore management. Despite a
plethora of available dressings, growth factors, and adjunctive therapies, there is no strong evidence to indicate that
any given wound care regimen is superior, and as a consequence. none has become dominant.4 Enzymatic debridement
ointments have been in use since the 1950s and continue to
be a valuable tool. Negative pressure wound closure devices
increasingly have been used for pressure sores. A recent
Cochrane review, however, found that while the data do
demonstrate a beneficial effect of wound healing, more quality research is needed before confirming it as a mainstay of
pressure wound treatment.25
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