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15 - Musculoskeletal and Connective Tissue Disorders |
457
activity warrants earlier use of combination
DMARD therapy or biologic response modifier
(BRM) therapy.
The ACR guideline summarized the
evidence guiding appropriate use of nonbio-
logic DMARDs and BRMs, which are classified
as anti-tumor necrosis factor alpha (anti-TNFα)
agents and other non-TNFα BRMs.
97
More long-
term evidence exists for the DMARDs than for
the BRMs. Treatment recommendations are
dependent on duration of disease activity (early
RA is <6 months; established RA is ≥6 months),
disease activity (low, moderate, or high), and
presence of poor prognostic factors. Poor prog-
nostic factors include one or more of functional
limitations, extra-articular disease (e.g., pres-
ence of rheumatoid nodules, RA vasculitis, Felty
syndrome), positive rheumatoid factor or anti–
citrullinated protein antibody, or bony erosions
by radiograph.
The DMARDs are used singularly or
combined depending on disease activity and
prognostic factors, with more aggressive therapy
used with more severe RA.
97
Most DMARDs take
several weeks before onset of full therapeutic
benefit and have limited durations of efficacy.
A 3-month trial is recommended before making
decisions to alter therapy with DMARDs or anti-
TNFα; 6 months for non-TNFα BRMs. If mono-
therapy does not get and keep a patient at goal
of low disease activity or remission, then addition
of a different DMARD (i.e., methotrexate, lefluno-
mide, or hydroxychloroquine) is warranted. If one
to two combinations of DMARDs do not achieve
and maintain the patient at goal, then the DMARD
is changed to or combined with a BRM.
All BRMs can be used as monotherapy with
the exception of infliximab, which should always
be paired with methotrexate.
97
Rituximab can
be used when patients have poor prognostic
factors, have failed other therapies, or who have
had a malignancy within the past 5 years. Combi-
nations of biologic therapies are not supported
by current evidence.
Because DMARDs and BRMs can take
weeks to months to achieve maximum effect,
glucocorticoids and NSAIDs can be used for
short-term pain management. Glucocorticoids
differ from NSAIDs by having both disease-modi-
fying and anti-inflammatory properties. Gluco-
corticoids should be used at a low dose (5 mg/
day or less) for limited courses of therapy; only
rarely is long-term use warranted.
98
Low-dose
glucocorticoids are used as adjunct therapy
for pain and inflammation control or for bridge
therapy while making changes in DMARD or
BRM therapies. Short-term high-dose bursts can
be used for acute flares. Glucocorticoids can
also play an important role in withdrawal of BRM
and DMARD therapy in patients in remission.
99
NSAIDs
can help with pain and inflammation;
they do not have disease-modifying activity.
Risks
and benefits should be weighed, especially in
patients with cardiovascular disease risks, renal
dysfunction, or GI ulcers or bleeds.
100
Disease
activity measures help quantify current disease
activity, select medication choice and numbers
of agents to use, and identify when a patient is
in remission.
101
There are several different tools
that have been validated to monitor and quan-
tify disease activity. When a patient responds to
therapy with sustained low disease activity or
remission, downward titration and even removal
of the BRM is supported by evidence.
102,103
Review of Evidence Base
Supporting Treatment
Recommendations for Older Adults
Because older patients with RA have typically
had the condition for many years, the disease
is often further progressed, with greater impact
on function. The standard RA treatment for
older adults is the same as other adults, and
few data are specific to older patients. Older
adults respond to DMARD and BRM therapies
in a way that is comparable to younger adults.
104
A rapidly-administered patient questionaire,
such as the Multi-Dimensional Health Assess-
ment Questionaire, can be at least as indicative
of treatment response and may replace more
complex assessments of response that include
laboratory parameters and physical examina-
tion.
105
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Older patients tend to have more comor-
bidities that can influence RA medication selec-
tion. Anti-TNFα therapies can increase risk of
lymphoma.
106
They should be avoided in people
with a history of malignancy within the past 5
years. Anti-TNFα therapies also should not be
used in patients with New York Heart Association
class III or IV heart failure or with ejection fraction
<50%.
97
In patients with untreated hepatitis B or
treated hepatitis Child-Pugh class B or higher,
BRMs should be avoided. In RA patients with
hepatitis C, etanercept can be used.
Prior to initiation of BRMs, all patients should
be screened for latent tuberculosis (TB) infec-
tions. The tuberculin skin test can be used in
most patients. If someone has a history of a posi-
tive test, the interferon-ϒ–release assays are the
preferred screening test. If either test is positive,
the patient should also be screened with a chest
radiograph and if that is positive, then a sputum
assessment. If the patient has TB, TB therapy
should be completed before initiating biologic
therapy.
97
Evidence supports a link between the inflam-
matory processes of RA and those of cardiovas-
cular disease.
107
In particular, T-lymphocytes are
involved in both processes. People with RA have
a higher risk of myocardial infarction, with a rate
increase similar to diabetes. High-dose gluco-
corticoids (>7.5 mg/day) can increase blood
pressure and cardiovascular risks. Anti-TNFα
therapies and methotrexate might have positive
benefits for both RA and cardiovascular disease.
The natural course of aging can decrease
immune response. RA and associated medica-
tions can further increase the risk of infection.
Glucocorticoids have increased infection and
hospitalization rates when used for RA.
108
When
used short term at a low dose (≤5 mg/day),
glucocorticoids can produce anti-inflammatory
and disease-modifying effects and cause fewer
adverse effects.
98
At higher doses or longer dura-
tions, the significant side effect profile, especially
impact on bone density, glaucoma, weight, and
metabolic system, should be weighed against
advantages.
17,109
Older adults with RA should receive immu-
nizations for influenza, pneumococcus, and
hepatitis B.
97
For the pneumococcal vaccine, this
should be given once after age 65. If the person
received a prior pneumococcal vaccine before
age 65, and it has been at least 5 years, that
person should be revaccinated once. An older
adult with RA starting DMARD therapy should be
vaccinated for herpes zoster. If an older adult is
already on DMARD therapy and has not been
vaccinated, all vaccines can be given. If an older
adult is already on any BRM, the herpes zoster
vaccine is not recommended.
Medication regimen monitoring and adverse
effect management are integral parts of therapy
with immune modulating therapies. In particular,
complete blood count, liver function tests, and
renal function monitoring are important for most
of these agents. Both RA and glucocorticoids
are independent risk factors for osteoporosis,
warranting DXA evaluations of bone density
and considerations for osteoporosis preven-
tion or treatment medications. Specific medi-
cation monitoring recommendations should be
followed.
Common Problems Encountered
When Treating Older Adults with
is Condition
Older adults do not always receive RA therapy as
comprehensive or aggressive as their younger
counterparts. Studies of attitudes and priorities
have demonstrated older adults often select
therapy options with fewer daily side effects,
even if there are longer-term risks.
104
Rheumatol-
ogists and patients prioritize therapy consider-
ations differently.
110
Open communication about
options can help patients and providers find
common goals and strategies.
Fatigue is a common sequela
of RA that can
have a significant impact on function in older
adults. Physical activity and psychosocial inter-
ventions have been demonstrated to have a
benefit in helping manage fatigue.
111
RA is a progressive disease that leads to
loss of muscle tone and function over time, as
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15 - Musculoskeletal and Connective Tissue Disorders |
459
does aging. So, when flares, fractures, illness,
or hospitalization cause weakness, it takes
even longer in older patients to regain func-
tion. Ability to perform ADLs, participation in fun
activities, need for personal help and assistive
devices, and transportation issues contribute to
the total picture of RA care. Exercise and coor-
dinated interventions can help maintain func-
tion, decrease pain, and enhance quality of life.
Components of interventions demonstrated to
have success include group education, self-
management, upper extremity–focused exercise
instruction, and maintenance of a home exer-
cise regimen.
112
Yoga and tai chi have also been
shown to help maintain function and improve
psychosocial aspects of RA management.
113,114
Several oral health and GI implications exist
with both RA and its treatment.
115
The temporo-
mandibular joint is one of the joints that can be
impacted by RA. Glucocorticoids and bisphos-
phonates can increase risk of jaw osteonecrosis.
Hand and jaw RA can make it difficult for patients
to practice good oral hygiene. Attention to oral
care can improve oral health, quality of life, and
self-esteem. Constipation is a common problem
for older adults even without concomitant
medical conditions. Decreased physical activity
due to RA, decreased total body water, and
altered nutritional and fluid intake are contributing
factors. Opioids are well known for constipation
as a side effect; thus, treatment benefit needs to
be greater than adverse effects. If used, therapy
should only be for a short period (<6 weeks) with
preventative measures for constipation and fall
risk employed.
116
With age often comes an accumulation of
medical conditions with multiple implications on
therapy. For instance, some older adults might
not be surgical candidates, thus eliminating joint
replacement as a therapeutic option. In addi-
tion, depression is common with any chronic
condition, especially musculoskeletal disor-
ders. Anemia is a common comorbidity, and the
fatigue of RA and anemia further contribute to
the difficulties of managing RA and other comor-
bidities and differentiating causative factors.
117
P R
G C A
Etiology, Epidemiology, and
Clinical Presentation Specic to
Older Adults
Although the exact causes of PMR and giant cell
arteritis (GCA) are unknown, pathophysiology
might be related to aging, the immune system,
decreasing endocrine function, genetics, and
environmental factors.
118-121
These diseases
predominantly affect older adults (>50 years)
with average onset at 73 for PMR
118
and 70 for
GCA.
121
Women and whites are more likely to
develop PMR and GCA.
120,121
The annual inci-
dence of PMR and GCA is 53 and 19 patients
per 100,000 people, respectively.
119
PMR symptoms are moderate to severe
muscle aches and morning stiffness of the torso
(e.g., neck, shoulders, pelvis) or upper and lower
extremities that last for greater than 45 minutes
and persist longer than 2–8 weeks.
118-120
Patients
can experience fatigue, decreased energy,
weakness, weight loss, anemia, and sometimes a
slight fever and depression. Joints are usually not
swollen, but up to 25% can have joint synovitis.
Symptoms can begin unilaterally but generally
progress to bilateral appearance. They can be
worse in the morning or after extended periods
of sitting or lying down and can begin quickly
or gradually. The disease can remit within 1 to 2
years without therapy. About 50% of patients will
have a relapse after initial treatment.
119
GCA (also known as temporal arteritis) can
occur alone or present with PMR (up to 60% of
patients), whereas only 16% to 21% of patients
with PMR have concomitant GCA.
118-121
Symp-
toms include new headache, which is usually
severe and near the temples, fever, anorexia,
weight loss, depression, tender scalp, pain
with chewing, jaw discomfort, tongue pain, loss
of taste, and visual change. Patients with GCA
can also experience swollen, inflamed, and red
temple, neck, or arm arteries. Blindness some-
times occurs and is a medical emergency.
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Besides physical examination, a shoulder
and hip ultrasound to document bursitis or
synovitis and some laboratory tests to docu-
ment an inflammatory process will be helpful to
rule in PMR and rule out other conditions.
118,120
In PMR patients, generally the ESR (>30–
50 mm/hr), platelet count, and C-reactive protein
(>6 mg/dL) will be elevated; hemoglobin will be
decreased with a mild, normochromic, normo-
cytic anemia; and the rheumatoid factor will be
negative. Sometimes a MRI or positron emis-
sion tomography scan are obtained. The ESR is
elevated in GCA also. A temporal artery biopsy
will be obtained to confirm GCA.
120,121
KEY POINT:
e symptoms for
polyarthralgia rheumatica and GCA are similar
to other disorders, making diagnosis dicult.
Summary of Standard Treatment
and Review of Evidence
Base Supporting Treatment
Recommendations for Older Adults
Because these conditions occur mostly in
older adults, very few differences exist for
treatment of older adults versus middle-aged
adults. Glucocorticoids are considered first-line
therapy for PMR because NSAIDs are usually
inadequate.
118-120
The starting prednisone dose
is 15–20 mg daily for 2–4 weeks. In the past,
quick response to glucocorticoids was a hall-
mark of PMR diagnosis, but newer data docu-
mented that up to 4 weeks can be required for
complete response, which is achieved in only
70% of patients. During treatment initiation, the
ESR should return to baseline, and if it does
not, a different disease diagnosis should be
considered. After 2–4 weeks, the oral glucocor-
ticoids are then tapered. One tapering method
is to decrease the daily dose by 2.5 mg every
2–4 weeks until 10-mg daily dose.
118
This 10-mg
dose is used for 1 month and then the daily
dose is decreased by 1 mg every month until
discontinuation or flare-up. Some prescribers
use a slower taper, decreasing the dose over
longer durations; thus, treatment can last for 1–2
years. Sometimes symptoms reappear, requiring
extended duration of treatment. Methylpredniso-
lone 120 mg intramuscularly every 3–4 weeks
can be used, tapered by 20 mg every 2–3
months. Methotrexate, a steroid-sparing agent, is
sometimes added in the attempt to decrease the
long-term steroid dose and improve response;
however, the data were mixed, and one study
showed positive short-term effects but no differ-
ence in long-term benefits.
118
Subsequent flares
can be treated with the prednisone dose that
initially controlled the disease with or without
methotrexate added. Other immune-modulating
medications are being explored but not recom-
mended as first-line therapy.
The glucocorticoid therapy for GCA is
higher (40–60 mg prednisone per day; about
0.7–1 mg/kg) than PMR, and it is preferably
started after the biopsy but should not be
delayed if biopsy is scheduled for a couple
days later.
119-121
Response should be seen within
24–72 hours.
119
Similar to PMR, after 2–4 weeks
of symptom remission, a slow taper is begun;
about 10% decrease every 2–3 weeks until 10
mg daily followed by decreasing the dose 1 mg
per day each month until discontinuation, which
is usually 18–24 months after initiation. Metho-
trexate does not have a rapid onset of action
but is effective for this condition. Therefore, this
medication is generally reserved for relapses or
patients with significant glucocorticoid adverse
effects. TNFα inhibitors might be used in long-
standing refractory GCA cases. Mixed results
exist for the inclusion of low-dose aspirin to
prevent GCA complications.
Common Problems Encountered
When Treating Older Adults with
is Condition
Glucocorticoids are associated with many
adverse effects experienced by 65% to 81%
of those with PMR
118
and 25% to 50% (serious
effects) of those with GCA.
121
They can cause
osteoporosis (as discussed),
86,87
myopathies, and
hypogonadism. Glucocorticoids can also cause,
hasten progression, or worsen other comor-
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15 - Musculoskeletal and Connective Tissue Disorders |
461
bidities such as diabetes, cataracts, glaucoma,
hypertension, and infection in some older adults,
frequently requiring initiation or dose adjustment of
medications for these conditions.
They are asso-
ciated with wasting/weakening of muscles, liga-
ments, tendons, and skin; drug-induced Cushing
syndrome; and peptic ulcers. Many psychological
adverse effects exist with these medications, with
some of the medication-induced negative mood
and behavior therapies compounding underlying
depression and potential behavior problems
in patients with Alzheimer disease. Glucocorti-
coids can increase GI bleeding risk secondary
to medication-related peptic ulcer formation.
Concomitant NSAIDs can further compound this
risk. If long-term glucocorticoid use is warranted
and prescribed with concomitant NSAIDs, a PPI
might reduce GI bleeding risk. Ensuring older
adult vaccinations are up to date is good practice
before or early during long-term glucocorticoid
therapy.
119
Careful monitoring of an older adult is
required to identify and resolve glucocorticoid-
induced adverse effects.
P U
Etiology, Epidemiology, and
Clinical Presentation Specic to
Older Adults
The older and more frail the patient, the higher
the risk for pressure ulcer development. Pres-
sure, shear, and friction are the three major
factors in the formation of pressure ulcers.
Patients older than 70 are at a greater risk for
pressure ulcers.
122
Additional factors, some of
which have a higher prevalence in older adults,
are found in Table 15-3.
123,124
Critical care patients are at particularly high
risk with a direct relationship with mechanical
ventilation.
125
The Braden scale
126
and the Norton
scale
127
are two common scales used to predict
pressure ulcer risk. Albumin is a laboratory
parameter that can assist in the assessment of
pressure ulcer risk, which needs to be adjusted
for dehydration when interpreting results.
128
Pressure ulcer prevalence is approximately
12% to 13%.
129
The mean age of people with pres-
sure ulcers is 72–73 years. The most common
pressure ulcer sites are the heel, coccyx, and
ear.
130
Pressure ulcers are defined by stages
indicating depth and severity. Stages range from
I to IV, with additional categories for unstage-
able and suspected deep-tissue injury; see the
National Pressure Ulcer Advisory Panel (NPUAP)
website for pictures.
131,132
Staging is based on
the amount of tissue loss that has occurred, with
stage IV representing full tissue loss to the point
of bone, tendon, or muscle exposure.
Table 15-3. Factors Associated with
Pressure Ulcers
Age over 70
Altered sensory perception
Altered mental state
Inability to perceive pressure
Comorbidities: diabetes, malignancy, stroke,
heart failure, hypertension, renal failure,
anemia, impaired circulation, urinary and fecal
incontinence, lymphopenia
Infection (sepsis, fever, pneumonia)
Emergency department stay
Longer length of stay in a facility
Malnutrition (hypoalbuminemia)
Male gender
White or black race
Current smoking
Physical restraints
Dry and scaly skin or excessive skin moisture
History of pressure ulcers
Decreased activity level
Immobility or inability to reposition
Weight loss or low BMI
Surgical intervention
Critical care, especially if receiving mechanical
ventilation
BMI, body mass index.
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Pressure ulcers have a significant impact on
quality of life.
133
Presence and treatment of pres-
sure ulcers can lead to changes in environment
such as a pressure-reduction bed, infringement
on personal time, negative impact on sexual
activity, loss of autonomy with function, and social
isolation. Pressure ulcers are associated with
pain, can lead to emotional difficulties including
depression, have negative financial impact, and
are associated with increased mortality.
Summary of Standard Treatment
Pressure ulcer care starts with prevention. The
cost of treatment of a stage IV pressure ulcer far
exceeds the cost of pressure ulcer prevention
and early identification programs.
130
Preventive
techniques include avoiding or minimizing fric-
tion when changing positions, changing positions
regularly, keeping skin clean and dry (proper
incontinence care is particularly important), and
avoiding vigorous massage (shear).
134
For those
patients that can, position shifts should occur
at least every 15 minutes.
134
For those patients
who cannot, use of a mattress that redistributes
weight is recommended with repositioning at
least every 2 hours. Many available interven-
tions, such as pressure-relieving boots, eleva-
tion of the head of the bed, foam supports with
holes or indentations at boney prominences, and
mattress overlays, are also available to decrease
pressure on common pressure points (heels,
coccyx, ischium, trochanter, shoulders, knees,
ankles, and elbows) based on the contour of the
human body.
135
Good nutrition is another key to
pressure ulcer prevention and wound healing.
A balanced diet with supplements as needed
is the minimum level of nutrition intervention
required.
136
The 2009 NPUAP pressure ulcer guide-
lines
131
can be used along with information from
the 2008 guideline for pressure ulcers in long-
term care.
137
A protocol for the treatment of
pressure ulcers can be found in Figure 15-2.
135
This protocol involves steps to prevent, identify
early, stage, monitor, treat, and resolve pres-
sure ulcers. A multifactorial approach such as
the one presented in Figure 15-2 plus treat-
ment of concomitant conditions is essential for
successful pressure ulcer resolution. Treatment
involves debridement, cleansing, and dressing
of the wound. Management of bacterial load is
another important element. This should be done
with debridement whenever possible, but anti-
biotics can be considered when debridement
alone is not effective.
Wound debridement can be done in several
different ways depending on the nature of the
wound. For quick debridement, surgical (also
known as sharp) debridement is typically used.
Wet to dry debridement can be effective but
does not differentiate healthy from unhealthy
tissue well, so use has declined. Enzymatic
debridement targets and digests the extracel-
lular proteins in the unhealthy tissue.
The pharmacologic treatment of pressure
ulcers is primarily in the dressing phase.
122,138
The therapeutic goals are to maintain a moist
wound environment, maintain bacterial balance
between colonization and overgrowth/infection,
and remove necrotic tissue with debridement
(see Table 15-4).
139,140
More than 300 different
products are available, including transparent
films, hydrocolloids, alginates, foams, hydro-
gels, and hydrofibers. The choice of dressing
is primarily driven by the moisture status of the
wound. Transparent bio-occlusive films maintain
the moisture already in the wound. Hydrocol-
loids do not allow moisture to escape the wound.
Hydrogels and hydrofibers provide some mois-
ture to the wound and are best in wounds that
need only moisture to heal. They absorb a limited
amount of excess moisture but assure the wound
stays moist. Foam dressings are very absorbent
and are especially helpful for deep or oddly
shaped wounds. Alginates are specifically bene-
ficial with bloody exudative wounds or infected,
draining wounds.
Pressure ulcer care can be associated with
significant discomfort.
140
Therefore, pain control
is a key factor in the treatment of pressure ulcers,
especially during dressing changes or debride-
ment, where pretreatment with an analgesic
might be required.
135
Appropriate pain control
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David: can you crop the last two lines (copyright info) off of
Fig. 15-2?
Figure 15-2. Aspects of care for pressure ulcers.
Source: Reprinted with permission from Sibbald RG, Goodman L, Norton L, et al. Prevention and treatment of
pressure ulcers. Skin Therapy Lett. 2012;17:7.
would ensure the patient can move to relieve
pressure, if physically able. Oversedation can
further increase pressure ulcer risk.
124
Appropriate antibiotic use is a key compo-
nent of pressure ulcer healing. Systemic antibi-
otics are appropriate if clinical signs of infection
exist, such as elevated fever, elevated white
blood cell count, or red and swollen surrounding
tissue.
139
However, routine cultures of the wound
bed do not yield useful results in directing anti-
biotic selection. Topical antibiotics are usually
not recommended, with the possible excep-
tion of superficial infections.
138
For deep tissue
infections, including osteomyelitis, intravenous
systemic antibiotics are required.
The seriousness of pressure ulcers and the
need to prevent, identify early, and treat effec-
tively are emphasized by many leading health-
care agencies. The Institute for Health Care
Improvement, Centers for Medicare & Medicaid
Services (CMS), the NPUAP, and the Surgeon
General’s Healthy People 2020 are a few. The
National Quality Forum with CMS has designated
stage III and IV ulcers acquired in the hospital as
“never errors,” which are serious and expensive
medical errors that should never occur.
141
CMS
will reduce or not pay for hospital stays due to
these hospital-acquired ulcers.
Common Problems Encountered
When Treating Older Adults with
is Condition
Many people over 65 have accumulated
comorbid conditions and other variables asso-
ciated with increased pressure ulcer risk. Medi-
Prevention & Treatment of Pressure Ulcers
• Determine Healability
T reat the Cause
• Pressure & shear
• Moisture & friction
• Nutrition
• Mobility
Patient-Centered Concerns
• Pain control
• Bed rest is harmful
• Smoking cessation
• Activities of daily living
Local Wound
• Location
• Length, width, depth
• Level (grade, stage)
Debridement
• Surgical
• Autolytic
• Mechanical
• Enzymatic
• Biological
Infection
• 3 NERDS criteria = topical Tx
• 3 STONEES criteria = systemic Tx
Inflammation
• Bedside protease test
Moisture Balance
• Foams
• Calcium alginates
• Hydrogels
• Hydrocolloids
• Films
Edge Effect: Stalled Chronic Wound
• Electrical stimulation, ultrasound
• Hyperbaric oxygen
• Negative pressure wound therapy
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| Fundamentals of Geriatric Pharmacotherapy
Table 15-4. Modern Classes of Dressings
Class Description
Tissue De-
bridement Infection
Moisture
Balance
Indications/
Contraindications
1. Films/
membranes
Semipermeable adhesive
sheet; impermeable to
water molecules and
bacteria.
+ – – Moisture vapor
transmission rate varies
from film to film. Should
not be used on draining
or infected wounds.
a
Create occlusive barrier
against infection.
2. Nonadherent Sheets of low adherence
to tissue. Nonmedicated
tulles.
– – – Allow drainage to seep
through pores to
secondary dressings.
Facilitate application of
topical.
3. Hydrogels Polymers with high water
content. Available in
gels, solid sheets, or
impregnated gauze.
++ –/+ ++ Should not be used on
draining wounds. Solid
sheets should not be
used on infected wounds.
4. Hydrocolloids May contain
gelatin, sodium
carboxymethylcellulose,
polysaccharides, and/or
pectin; sheet dressings
are occlusive with
polyurethane film outer
layer.
+++ –/+ ++ Should be used with care
on fragile skin. Should
stay in place for several
days. Should not be used
on heavily draining or
infected wounds.
a
Create
occlusive barrier to
protect the wound from
outside contamination.
Odor may accompany
dressing change and
should not be confused
with infection.
5. Acrylics Clear acrylic pad enclosed
between two layers of
transparent adhesive
film.
+++ –/+ ++ Use on low- to moderately
draining wounds where
dressing may stay in
place for extended time.
May observe wound
without changing.
6. Calcium
alginates
Sheets or fibrous ropes of
calcium sodium alginate
(seaweed derivative);
have hemostatic
capabilities.
++ + +++ Should not be used on
dry wounds. Low tensile
strength: avoid packing
into narrow deep
sinuses. Bioresorbable.
7. Composite
dressing
Multilayered, combination
dressings to increase
absorbency and
autolysis.
+ – +++ Use on wounds where
dressings may stay in
place for several days.
a
8. Foams Nonadhesive or adhesive
polyurethane foam; may
have occlusive backing;
sheets or cavity
packing; some have
fluid lock.
– – +++ Use on moderately to
heavily draining wounds.
Occlusive foams should
not be used on heavily
draining or infected
wounds.
a
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15 - Musculoskeletal and Connective Tissue Disorders |
465
9. Charcoal Contains odor-absorbing
charcoal within product.
– – + Some charcoal products
are inactivated by
moisture. Ensure dressing
edges are sealed.
10. Hypertonic Sheet, ribbon, or gel
impregnated with
sodium concentrate.
+ + ++ Gauze ribbon should not
be used on dry wounds.
May be painful on
sensitive tissue. Gel may
be used on dry wounds.
11. Hydrophilic
fibers
Sheet or packing
strip of sodium
carboxymethylcellulose;
converts to a solid
gel when activated by
moisture (fluid lock).
+ – +++ Best for moderate amount
of exudates. Should not
be used on dry wounds.
Low tensile strength:
avoid packing into the
narrow deep sinus.
12. Antimicrobials Silver, iodides, PHMB,
honey aniline dyes with
vehicle for delivery:
sheets, gels, alginates,
foams, or paste.
+ +++ + Broad spectrum against
bacteria. Should not be
used on patients with
known hypersensitivities to
any product components.
13. Other
devices
Negative-pressure
wound therapy applies
localized negative
pressure to the surface
and margins of wound.
– + +++ This negative pressure–
distributing dressing
actively removes
fluid from wound and
promotes wound edge
approximation. Advanced
skill required for patient
selection for this therapy.
14. Biologics Living human fibroblasts
provided in sheets
at ambient or
frozen temperature;
extracellular matrix.
Collagen-containing
preparations; hyaluronic
acid, platelet-derived
growth factor.
– – – Should not be used on
wounds with infection,
sinus tracts, or
excessive exudate or on
patients known to have
hypersensitivity to any of
the product components.
Cultural issues related
to source. Advanced
skill required for patient
selection for this therapy.
PHMB, polyhexamethylene biguanide.
a
Use with caution if critical colonization is suspected.
– no activity
+ minimal activity
++ moderate activity
+++ strong activity
Source: Reprinted with permission from Sibbald RG, Goodman L, Woo KY, et al. Special considerations in
wound bed preparation 2011: an update. Adv Skin Wound Care. 2011;24:431-432, ©Lippincott Williams &
Wilkins 2011.
Class Description
Tissue De-
bridement Infection
Moisture
Balance
Indications/
Contraindications
Table 15-4. (cont’d)
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466
| Fundamentals of Geriatric Pharmacotherapy
cations can also decrease mobility, alter perfu-
sion, alter sensation, or negatively impact wound
healing. Specific medication classes to avoid
or at least carefully monitor in patients with high
pressure ulcer risk include glucocorticoids,
sedative/hypnotics, opioids, antipsychotics,
tricyclic antidepressants, and antihypertensives.
Prevention, identification, and treatment of
pressure ulcers have always been a challenge,
especially when caring for frail older adults. The
prevalence of pressure ulcers in a healthcare
environment is an indicator of care quality. Those
who audit or pay for care scrutinize both the
frequency of pressure ulcer development as well
as the effectiveness of wound healing programs.
Pressure ulcer treatment requires addressing
all of the many factors associated with risks,
response to care, and caregiver and provider
issues. This frequently requires interprofes-
sional teams. Pharmacist participation on such
teams has been demonstrated to contribute to
improved patient outcomes.
123
KEY POINT:
Because prevention is
the rst step to pressure ulcer treatment
planning, patients should be immediately
assessed on institutional placement or
ambulation change of any kind.
Nutritional status and skin checks are both
essential components of the prevention or treat-
ment plan.
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