Geriatrics and Gerontology
Pressure Ulcer Management in the Geriatric Patient
Patricia L Orlando
OBJECTIVE: To increase the understanding of pharmacists and other
health-system clinicians regarding pharmaceutical applications of
pressure ulcer prevention and treatment in geriatric patients.
DATA SOURCES: An extensive MEDLINE retrieval was conducted
which encompassed the years 1967–1998; the search terms used
included pressure sore, pressure ulcer, decubitus ulcer, and
geriatrics.
DATA SUMMARY: Pressure ulcers affect populations with limited
mobility, reduced cognition, and less-independent activities of daily
living, such as the elderly. Identification of the high-risk patient is
required for successful prevention outcomes. For existing lesions, a
variety of treatment modalities exist, not all of which have
demonstrated therapeutic benefit. Given these options, clinicians are
faced with treatment selection challenges that should be based on
the clinical setting, available scientific evidence, and individualized
patient care needs.
CONCLUSIONS: Prevention of pressure ulcerations is imperative to
reduce patient morbidity, mortality, and overall healthcare costs.
Given the number of treatment options available, pharmacists can
assist in the treatment selection process. Education of the patient and
family regarding pressure ulcer prevention and treatment requires
early and ongoing involvement by the interdisciplinary team.
KEY WORDS: pressure ulcers, geriatrics, decubitus ulcers.
Ann Pharmacother 1998;32:1221-7.
PRESSURE ULCERS are skin lesions caused by increased
pressure over a bony prominence such as the sacrum, is-
chium, trochanters, ankles, or heels, which damage under-
lying tissues. These lesions, which are easily preventable,
occur as a result of infrequent repositionings of immobi-
lized patients, such as geriatric individuals, those with
stroke, dementia, spinal cord injury, and uncontrolled pain.1
Although known by a variety of names, the term “pressure
ulcer” has been designated by the 1989 National Pressure
Ulcer Advisory Panel (NPUAP) as the correct terminology
for these wounds.2 Other, less conventional terms include
pressure sores, bedsores, and decubitus ulcers.
Pressure ulcer prevalence for geriatric patients in nurs-
ing homes ranges from 2.6% to 24%.3 Geriatric orthopedic
Patricia L Orlando PharmD, Assistant Professor (Clinical), College of Pharmacy,
University of Utah, 258 Skaggs Hall, Salt Lake City, UT 84112, FAX 801/585-
6160
Reprints: Patricia L Orlando PharmD
The Annals of Pharmacotherapy
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patients, having a 66% incidence, represent one of the
highest risk groups for pressure ulcer development.4
Considering that the development of pressure ulcers is
preventable, costs associated with their management are
substantial and difficult to quantitate. Cost estimates have
ranged from $4000 to $40 000, depending on ulcer stag-
ing.5
Risk Factors
The primary risk factor for the development of a pres-
sure ulcer is elevated pressure between a bony prominence
and external surface, with secondary risks including fric-
tion, moisture, shearing forces, and temperature.6
Age-associated skin changes may also enhance pressure
ulcer development. Morphologic epidermal skin changes
that occur during normal aging include depressed epider-
mal thickness, reduced numbers of melanocytes and Lan-
gerhans’ cells, and decreased vertical height with elevated
surface area of keratinocytes and flattened dermoepider-
mal junctions. An atrophic dermis includes decreased
numbers of fibroblasts and mast cells with a less efficient
papillary capillary network.7 Aging skin demonstrates en-
hanced susceptibility to blister formation, increased poten-
tial for tear-type injuries, increased potential for deep tissue
injuries and infection, slower wound healing, easy bruis-
ability, attenuated microvasculature, and diminished elas-
ticity.1
Medications that depress central nervous system activity
potentially increase the patient’s risk for immobility. These
agents, which include sedative/hypnotics, narcotic and
nonnarcotic analgesics, anesthetics, tricyclic antidepres-
sants, antipsychotics, antianxiety drugs, and antiemetics,
may reduce sensory perception and cognitive awareness
while compromising opportunities to produce pressure re-
lief. Agents that lower the blood pressure may also reduce
mobility as well as tissue perfusion.8 Diuretics, for exam-
ple, may cause dehydration and impaired cognition in the
geriatric patient, enhancing the possibility of immobility.
Healing Environment
The physiologic process of wound healing is multifacto-
rial. Skin injury results in inflammation, which activates
■ 1998 November, Volume 32 ■ 1221
tissue complement. Increased capillary permeability oc-
curs with the accumulation of lymphocytes and neutro-
phils, which respond to an infection stimulus. Macro-
phages appear at the wound site 48–96 hours after the ini-
tial insult, performing the necessary debridement prior to
fibroblastic activity. Activated macrophages release inter-
leukin-1 (IL-1) and tumor necrosis factor-alpha, which are
involved with angiogenesis.9 Activated T-lymphocytes
also migrate into the inflammatory wound bed, releasing
such lymphokines as gamma interferon and transforming
growth factor-beta (TGF-β), which also contribute to an-
giogenesis.10 Macrophage secretory products may also in-
fluence fibroblastic activities such as chemotaxis, prolifer-
ation, and collagen synthesis.11
Clinical studies have demonstrated controversy regard-
ing benefit to wound healing with the supplementation of
specific nutrients in patients who are not deficient in those
nutrients. Zinc, which is used in protein synthesis, and vi-
tamin C (ascorbic acid), required for collagen synthesis,
are two nutrients commonly associated with wound heal-
ing. No studies have shown that the use of zinc in patients
who are not zinc deficient improves healing rates.12 Over-
use of zinc has been associated with impaired phagocyto-
sis and delayed wound healing.13 Collagen formation with
improved healing rates have been noted in patients supple-
mented with vitamin C.14 Any role that vitamin C may
have in the prevention of pressure ulcers remains to be de-
fined. The data to date suggest that a balanced diet, includ-
ing higher protein intake and vitamin and trace-mineral
supplementation, in clinically deficient patients is critical
to optimize the healing environment.13
Management
Once staging of the pressure ulcer is completed, based
on recommendations developed by the NPUAP15 and the
Panel on the Prediction and Prevention of Pressure Ulcers
in Adults (Agency for Health Care Policy and Research
[AHCPR]),16 the first aspect of treatment is to relieve pres-
sure from the wound site and to prevent the development
of other ulcers in areas of the newly distributed pressure.
To relieve the pressure in these unaffected areas, patients
should be repositioned every 2 hours, although the fre-
quency depends on the patient’s risk status and the support
surface.17 When the patient is repositioned to the side, the
back should be at a 30-degree angle to the supporting sur-
face to reduce pressure over the trochanter and malleolus,
using pillow supports and/or foam wedges. Doughnut cush-
ions should be avoided due to their potential to restrict per-
fusion to tissues in the center of the device.17
The patient’s skin should be inspected daily and kept
clean and moisturized. Bedclothes and linens should be
kept clean and wrinkle-free. Elbow and heel protectors
should be considered to cushion these bony prominences.
Lifting devices, such as a trapeze, can reduce friction and
shear during transfers.18
Many different pressure-relieving devices are available
on the market. Sheepskin and egg-crate foam mattresses
do not lower pressures adequately to prevent pressure ul-
cers.19 Foam mattresses, thicker than conventional egg
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crates, and static air mattresses are able to lower pressures
below capillary-filling pressures under bony prominences,
according to insufficient data reports.17 The fluidized bed
involves channeling warm air through small microspheres
to create a liquid “without wetness” to slow protein catab-
olism.20 For patients who are confined to a wheelchair, air-
filled cushions have been shown to produce the lowest lo-
calized pressure.1 Although pressure-relieving devices may
decrease the incidence of pressure ulcers, no one type of
device is any more effective than another to protect the pa-
tient’s skin.16
Debridement
Once the pressure is relieved, any necrotic tissue must
be debrided or removed from the wound. Debridement is
not necessary for stage I ulcers since the skin is intact. The
autolytic activity that occurs beneath the occlusive or
semipermeable dressing of a stage II wound is usually suf-
ficient debridement. Stage III and IV ulcers frequently
contain devitalized tissue that requires removal via surgical
instruments or by mechanical or autolytic methods. Some
debridements may be performed at the bedside with the
clinician using forceps and a scalpel. Some nursing facili-
ties may not have staff qualified to perform bedside de-
bridement, so patients have to be transported to the hospi-
tal. As a result, some patients may not receive adequate
surgical intervention. However, the patient and clinical
staff must remain vigilant about pressure-relieving mea-
sures since recurrence of the ulcers is possible.18
Mechanical debridement, which is effective for large,
deep wounds, is performed with gauze moistened with
NaCl 0.9%, which is reapplied every 6–8 hours, depend-
ing on the amount of wound drainage.18 These wet-to-dry
dressings are recommended for removal of superficial
necrotic tissue.9 The actual timing interval of the dressing
changes must be monitored carefully to avoid unnecessary
pain to the patient and to prevent impairment of epithelial-
ization, since viable tissue may also be removed during the
dressing change.18
Hydrotherapy with a whirlpool, shower, or pulsed water
system may be used as an adjunctive mechanical debride-
ment method.18 This technique can be helpful to loosen
hardened eschar, thick exudate, and loose necrotic tissue.
Autolytic debridement is accomplished by applying a
transparent adhesive, hydrocolloid, hydrogel, or semiper-
meable foam wafer to the wound. Tissue fluid containing
neutrophils, macrophages, and enzymes accumulates un-
der the dressing while necrotic material is removed. This
synthetic dressing is usually changed every 5–7 days.21
Chemical enzymatic agents, including collagenase
(Santyl), trypsin (Granulex), fibrinolysin and deoxyribonu-
clease (Elase), papain (Panafil), or sutilains (Travase) rep-
resent another method of debridement. These topical pro-
teolytic enzyme products hydrolyze superficial necrotic
matter and loosen eschar prior to surgical debridement.
Disadvantages associated with their use include the inabili-
ty to remove a hardened eschar or larger amounts of tissue
debris found in deeper wound beds, several applications
required for potential benefit, increased costs (compared

with wet-to-dry dressings), and damage to adjacent healthy
tissue.18 As granulation tissue develops, additional debride-
ment may not be necessary.
Postdebridement Wound Care
Many products are available on the market to potentially
enhance healing of pressure ulcerations. Gas-permeable
polyurethane films, applied to stage I and II ulcers, act like
“skin” to allow water vapor and gas transfer but prevent
moisture penetration. These dressings are changed weekly
depending on the amount of generated wound fluid.22 Ex-
amples include Tegaderm and Op-site.
Similar to the semipermeable films are the semiperme-
able polyurethane foams that absorb excessive wound de-
bris while maintaining a moist wound bed. This transpar-
ent formulation, recommended for uninfected stage II or
III ulcers, should not be used in ulcers that have eroded
into muscle. Examples include Allevyn and LYOfoam.18
Hydrocolloids are semipermeable or occlusive dressings
that help debride necrotic matter by autolysis. The hydro-
colloid interacts with the wound fluid to form a gel con-
sisting of bactericidal and growth factors to promote an-
giogenesis and granulation. The self-adhesive dressing is
changed every 5–7 days depending on the generation of
wound fluid.17 Hydrocolloids are recommended for unin-
fected stage II or III ulcers.21 Examples of hydrocolloids
include Duoderm and Tegasorb.
Hydrogels are composed of an aqueous or glycerin-
based gel between two layers of polyethylene film. When
the dressing is applied to stage II, III, or IV ulcers having
minimal-to-moderate exudate, the inner film is removed
and oxygen and water vapor are released into the wound
bed.23 Examples include Carrington Gel and Clear-site.
Alginate dressings, derived from seaweed, are highly
absorbent and conform to the shape of the stage III or IV
ulcer with heavy exudate.22,23 Examples include Kaltostat
and Sorbsan.
Antibiotics
When considering pressure ulcer management, clini-
cians frequently oscillate between infection and coloniza-
tion questions. Bacterial infection may be initiated by a
disruption in the skin barrier with erythema, fever, pain,
edema, pus, and/or a foul odor. However, the number of
bacterial organisms in a wound is not predictive of the
healing outcome. Wounds colonized with more than 106
organisms have healed without clinically relevant signs of
infection.24 Routine culturing of pressure ulcers in the ab-
sence of signs and symptoms suggestive of infection, even
in patients with known bacterial colonizers (including
methicillin-resistant Staphylococcus aureus), is question-
able.
Acute wounds tend to react differently to populations of
bacteria than do chronic wounds. Acute wounds tend to be
more susceptible to bacterial occupation. A chronic ulcer,
however, may exist in a symbiotic relationship with a large
number of bacteria without demonstrating any clinical
signs of infection.25 Generally, the patient must be evaluat-
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Management of Pressure Ulcers
ed against other criteria such as wound status (including
location, chronicity, wound size and depth, amount/color/
odor/viscosity characteristics of exudate with associated
saturation of dressings, tissue erythema, surrounding skin
color, maceration and induration, presence of sinus tracts,
amount of necrotic or granulation tissue, pain), impaired
healing, other underlying diseases, and current medica-
tions.
Infectious complications of pressure ulcers may include
localized infection, cellulitis of adjacent tissue, osteomyeli-
tis, and bacteremia. Osteomyelitis of the underlying bone
may be a cause of the delayed healing of the pressure ul-
cer. If not diagnosed, the osteomyelitis becomes a primary
risk for bacteremia and/or sepsis.26
Pressure ulcer-related osteomyelitis is generally polymi-
crobial. Cultured aerobic organisms include staphylococci,
enterococci, Proteus mirabilis, Escherichia coli, and Pseu-
domonas aeruginosa. Anaerobic bacteria may include pep-
tostreptococci, Bacteroides fragilis, and Clostridium spp.27
Bacteremia resulting from pressure ulcers is usually due to
P. mirabilis, E. coli, P. aeruginosa, Klebsiella spp., S. au-
reus, or B. fragilis.22 Swab cultures of the wound surface
are not a reliable means of identifying infecting organisms
due to colonizing bacteria. Antibiotic management of os-
teomyelitis should be based on carefully collected surgical
debridement cultures and/or bone biopsies with their asso-
ciated susceptibility data.28
Systemic antibiotics should be given when signs and
symptoms of infection are present (e.g., elevated leukocyte
count, fever, cellulitis with associated erythema and pain,
purulent wound discharge). The elderly, however, may
manifest less classical symptoms, such as confusion and
anorexia, with the onset of infection. Several different par-
enteral regimens have been used for patients with an in-
fected pressure ulcer or associated osteomyelitis, depending
on bone cultures and susceptibilities.27 Delivery of sys-
temic antibiotics to the infected pressure ulcer and associ-
ated osteomyelitis is less predictable in a patient with com-
promised vascular flow.
Topical antibiotics such as bacitracin, silver sulfadi-
azine, neomycin, polymixin B, and mupirocin may en-
hance local epidermal cell formation but may select for re-
sistant bacteria.29 Metronidazole, applied topically as a
0.75% gel or 1% lotion, to pressure ulcers has been studied
to control anaerobic colonizers.30 Clinical studies have yet
to demonstrate whether topical metronidazole improves
healing rates.
Topical antibiotics, generally, have not been shown to
improve clinical outcomes for patients with pressure ul-
cers, since healing can occur despite the wound not being
sterile.6 These products do not penetrate the wound bed
and may be helpful only to treat local surface infection.
The AHCPR guidelines, however, recommend that a 2-
week trial of topical antibiotics (silver sulfadiazine, triple
antibiotic) be considered for the clean, nonhealing pressure
ulcer, or for the wound that continues to have exudate de-
spite 2– 4 weeks of appropriate dressing care.16 The use of
topical antibiotics requires careful monitoring to avoid hy-
persensitivity reactions, toxicity due to absorption, and ad-
ditional costs.
■ 1998 November, Volume 32 ■ 1223
Other Management Approaches
Topical nitroglycerin, acting as a cutaneous vasodilator,
might play a role in pressure ulcer management. A case re-
port31 describes three elderly patients with varying degrees
of digital ulcerations due to several etiologies who were
treated with topical nitroglycerin 2% ointment. Follow-up
between 4 and 6 weeks showed complete healing of the ul-
cers with no adverse effects. In another study,32 54 patients
with anal fissures or anal ulcers were treated with nitro-
glycerin 0.3% ointment four times daily. After 8 weeks of
treatment, the wounds were healed in 77% of the patients
with anal fissures and 54% of those with anal ulcers. Ad-
verse effects included transient headache in 29% of the pa-
tients. Improved healing rates have also been noted in pa-
tients with arterial or venous ulcers treated with topical ni-
troglycerin.33
Despite the limited data that might favor the use of topi-
cal nitroglycerin, another study34 analyzed the effect of
topical nitroglycerin 2% ointment on transcutaneous oxy-
gen pressure (TcPO2), a noninvasive procedure that mea-
sures the tension of oxygen at a given skin or wound site to
determine whether a preventive technique for pressure ul-
cer management results in oxygen perfusion or anoxemia.
The results demonstrated a dose-related TcPO2 shunt up to
several centimeters away from the nitroglycerin applica-
tion site. Because no controlled trials have addressed the
use of topical nitroglycerin for pressure ulcer management,
caution must be exercised in this setting since the delicate
balance of available blood flow to the pressure ulcer could
be shunted to other healthier tissues. Additionally, the el-
derly may be more predisposed to adverse effects (i.e., hy-
potension and/or transient headaches), but this issue re-
quires study.
Topical phenytoin has been used in the healing of a vari-
ety of skin wounds.35 Although these studies contain de-
sign flaws, all have reported improved healing rates. Phen-
ytoin’s potential healing mechanisms may include fibro-
blastic proliferation, collagen formation, and reductions of
wound bacterial counts.35 Additional controlled studies are
required to understand the pharmacokinetics associated
with phenytoin regarding systemic absorption from vary-
ing wound depths. Although systemic absorption of the
topical application of phenytoin has resulted in subthera-
peutic serum concentrations (i.e., <10–20 mg/L), reported
adverse effects have included a transient burning sensa-
tion, skin rash, and hypertrophic granulation tissue.36 Other
adverse effects that have not been reported with topical
phenytoin, but occur with systemic administration, include
a rare hypersensitivity reaction with necrotizing hepatitis
and blood dyscrasias.35 Phenytoin may represent an alter-
native treatment for pressure ulcer management, but fur-
ther controlled trials are needed to verify this role.
Growth Factors
Growth factors are being studied as key mediators of the
wound healing process. These factors are produced by and
activate cells that are involved in healing (i.e., macro-
phages, platelets, fibroblasts, endothelial cells).37 Although
these agents have not received adequate clinical study in
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pressure ulcer management, an understanding of their gen-
eral function in wound care may shed light on any healing
applications for pressure ulcers.
Epidermal growth factor (EGF) stimulates epithelial
cells, fibroblasts, and keratinocytes during the healing pro-
cess. EGF accelerates epidermal regeneration and increas-
es tensile strength of incisions while enhancing wound
vascularization.37 Silver sulfadiazine cream combined with
EGF significantly (p < 0.02) accelerated healing rates of
partial-thickness skin burns and complex fracture grafts
compared with silver sulfadiazine cream alone.38 The de-
position of collagen involves synthetic and degradative
forces. Although type III collagen replaces and integrates
with existing fibrinogen in the wound, it is replaced by
type I collagen during healing.39 While EGF promotes
wound epithelialization, it also promotes, in vitro, fibro-
blasts to synthesize noncollagenous protein while impair-
ing the deposition of type I collagen during this healing
process.40 These findings are promising, but controlled hu-
man trials involving pressure ulcers are needed before the
use of EGF can be promoted in pressure ulcer management.
As a potent stimulator of fibroblasts, platelet-derived
growth factor increases the tensile strength of incisional
wounds. A single topical application to an incisional wound
can potentiate healing over 49 days.41 Platelet-derived
growth factor has been studied in diabetic foot ulcers and
pressure ulcers, with enhanced healing rates noted over 28
days.42 However, the control group also demonstrated im-
proved healing, which may have been due to excellent
hospital care. Another preclinical trial43 of 45 geriatric pa-
tients with pressure ulcers demonstrated improved healing
rates in patients receiving varying dosages of platelet-de-
rived growth factor. Similar trends have been noted in a di-
abetic foot ulcer sample.44 Preclinical results appear favor-
able for platelet-derived growth factor, but additional clini-
cal studies are warranted to determine the degree of
expected healing benefit in patients with pressure ulcers.
TGF-β, which includes two isoforms consisting of β1
purified from platelets and β2 purified from bone, en-
hances macrophage chemotaxis and type I collagen activity
and deposition within the wound.45,46 No data are available
regarding the impact of TGF-β on pressure ulcer healing.
Fibroblast growth factor stimulates epithelialization and
fibroblastic activities, and promotes granulation and angio-
genesis.47 A Phase I trial48 studied fibroblast growth factor
in paraplegic patients with pressure ulcers and showed an
increased healing rate at higher dosages. Preliminary work
suggests a role for fibroblast growth factor in pressure ul-
cer management, but additional studies are needed.
Insulin-like growth factor (IGF-1, IGF-2, or somato-
medins) is produced within the wound and is a mediator of
collagen synthesis due to its effects on fibroblasts.49 Al-
though research is ongoing, IGF is expected to play a role
in wound healing since growth hormone (a regulator of
IGF-1) has stimulated donor-site healing times.50
Keratinocyte growth factor, a member of the fibroblast
growth factor family, stimulates various skin-related struc-
tures such as hair follicles, sweat glands, and sebaceous
glands.51 Vascular endothelial cell growth factor stimulates
embryonic angiogenesis.52 Clinically relevant data regard-
 Management of Pressure Ulcers

ing these factors are sparse, so any role in pressure ulcer anecdotes, or inadequately designed studies in the litera-
management remains to be defined. ture. Table 157 provides an abbreviated summary of these
Considering the hematopoietic growth factors, granulo- various agents.
cyte–macrophage colony-stimulating factor, which stimu-
lates monocyte and granulocyte production as well as Summary
monocyte chemotaxis, has demonstrated improved healing
of incisional wounds in the rat model.53 Granulocyte colony- Given the myriad of treatment options for pressure ul-
stimulating factor, which increases circulating neutrophils, cers, a summary follows: stage I ulcers, consisting of a
showed no effects on healing. Additionally, the interleukins nonblanchable erythema, generally resolves once the pres-
(IL-1 and IL-2), which stimulate monocytes and T lym- sure is relieved. Stage II ulcers, consisting of a partial-
phocytes, have demonstrated enhanced healing trends.54,55 thickness skin loss, require pressure relief and a poly-
The roles of these various factors deserve more study to urethane dressing. Stage III ulcers, involving a full-thick-
determine their application in pressure ulcer management. ness skin loss, require debridement of devitalized tissue
Additionally, combination growth factor therapy may show using the wet-to-dry dressing technique. The hydrocolloid
a synergistic healing response.56 dressing, applied every 1– 4 days, is appropriate to main-
Clinical trial design is important to define the role of tain moisture in the wound bed while absorbing exudate.
growth factors in pressure ulcer management. Comparison Deeper stage III ulcers, as well as stage IV ulcers, require
groups need to be matched for ulcer staging as well as un- debridement. Wounds having less exudate require packing
derlying disease processes such as peripheral vascular dis- with less absorptive hydrogels, or NaCl 0.9%-soaked gauze
ease, nutritional status, and the absence of systemic or lo- packing. Moderate to heavy exudate requires dressings
cal wound infections. Patients with immunosuppressant with more absorptive capabilities, such as the hydrogels,
conditions such as diabetes, malignancy, or pregnancy, as alginates, or NaCl 0.9%-impregnated gauze.18
well as those who chronically use immunosuppressant Patient education regarding the prevention of pressure
drugs, such as prednisone, should be excluded. All groups ulcers should be incorporated into the treatment plan as
should receive appropriate wound care and surgical de- soon as the patient or caregiver is physically and mentally
bridement. Questions remain regarding growth factor as a able to do so. The primary goal of the education process is
monotherapy versus its combination with other antiinfec- to increase the patient’s and/or caregiver’s understanding
tive agents such as silver sulfadiazine cream or other growth of the disease process.58 Such programs have demonstrated
factors. Roles may also vary according to the use of growth a 63% reduction in pressure ulcer development for geri-
factors in different wound categories (e.g., stages II–IV atric hospitalized patients.59 The interdisciplinary team can
pressure ulcers, burns, diabetic foot wounds). Adequate also provide educational support for the patient and care-
follow-up time is crucial to determine optimal healing as giver with booklets supplied by the AHCPR (AHCPR
well as the occurrence of adverse reactions related to the Publications Clearinghouse, PO Box 8547, Silver Spring,
growth factors. Abnormal cell transformation, including MD 20907) and the NPUAP (SUNY at Buffalo, Beck
meta- or hyperplasia, is a current concern with growth fac- Hall, 3435 Main Street, Buffalo, NY 14214).
tor administration as noted in animal models.38 Methods of The pharmacist, working within the interdisciplinary
determining epithelial regeneration should also be outlined team, develops optimal pharmaceutical care applications
(e.g., use of serial photographs or punch biopsies) to docu- that emphasize patient risk factors; highlight pharmaceuti-
ment healing outcomes. Additional clinical trials are nec- cal products to promote the maintenance of healthy, intact,
essary to address these growth factor–related healing is- and moisturized skin; and provide recommendations re-
sues. garding appropriate nutritional support, the use of antispas-
A variety of other physical and topical applications for modic and antipsychotic agents, considerations for urinary
pressure ulcer management are presented as case reports, and/or bowel incontinence, and appropriate, cost-con-
scious antibiotic regimens for infected pressure ulcers.
Considering the holistic environment of pressure ulcer
management, the pharmacist monitors all aspects of drug
Table 1. Unconventional Agents Used in therapy to ensure that various goals of therapy are met dur-
Pressure Ulcer Treatments57 ing the healing process.
Topical agents
alcohol Burow’s solution gentian violet pectin
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EXTRACTO
OBJETIVO: Proveer un mayor conocimiento a los farmaceúticos y otros
profesionales del sistema de salud acerca de los productos farmaceúticos

para el tratamiento y prevención de úlceras causadas por presión en
pacientes geriátricos.
FUENTES DE INFORMACIÓN: Se hizo una búsqueda extensiva en el
MEDLINE y se seleccionó los años 1967–1998 buscando los términos
lesiones causadas por presión, úlcera de presión, úlcera de decúbito, y
geriatría.
RESUMEN DE DATOS: Las úlceras de presión son un problema serio que
afecta poblaciones con movimiento limitado, reducción cognositiva, y
menos independiente de las actividades del diario virir como la
población geriátrica. La identificación de los pacientes de alto riesgo fue
requerida para que los resultados fueran exitosos. A pesar de la variedad
de modalidades en tratamiento existente no todas han demostrado un
beneficio terapeútico en diferentes lesiones. Dada estas opciones, el
clínico se enfrenta a un reto en la selección de tratamiento que debe estar
basado en el escenario clínico, evidencia clínica disponible y las
necesidades individuales de cuidado en el paciente.
CONCLUSIONES: La prevención de úlceras de presión es imperativo para
reducir la morbilidad y mortalidad del paciente además el costo general
del cuidado en salud. Dado el número de las opciones de tratamiento
disponible, el farmaceútico puede ayudar en el proceso de selección. La
educación al paciente y familiares acerca de la prevención y tratamiento
de úlceras de presión requiere una temprana intervención y un
envolvimiento del grupo interdisciplinario.
WILMA M GUZMÁN
The Annals of Pharmacotherapy
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Management of Pressure Ulcers
RÉSUMÉ
OBJECTIF: Résumer l’information pertinente à la prévention et au
traitement des plaies de pression.
REVUE DE LA LITTÉRATURE: L’information a été recueillie par une
recherche dans la banque informatisée MEDLINE (1967–1998) en
utilisant les mots clés suivants: plaie de pression, ulcère de pression,
ulcère de decubitus, et gériatrie.
RÉSUMÉ: Les plaies de pression constituent un problème important chez
la population gériatrique. L’identification des patients à risque est
importante comme moyen de prévention. L’auteur décrit les différentes
modalités de traitement selon le type de plaies de pression. Chacune
comporte ses avantages et ses inconvénients.
CONCLUSIONS: La prévention des plaies de pression est importante pour
diminuer la morbidité, la mortalité, et les côuts de santé associés. Selon
le stade de la plaie de pression, le pharmacien peut suggérer différents
traitements. Le patient et les aidants naturels doivent être informés des
mesures de prévention et de traitement.
LOUISE MALLET
■ 1998 November, Volume 32 ■ 1227