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Transcript
ClinicalArticle
Clostridium difficile–
Associated Disease
Diagnosis, Prevention,
Treatment, and
Nursing Care
Maria E. Pelleschi, RN, MS, CCRN
This article has been designated for CE credit.
A closed-book, multiple-choice examination
follows this article, which tests your knowledge
of the following objectives:
1. Discuss the incidence of Clostridium
difficile–associated disease (CDAD) in the
critical care setting
2. Identify key preventive measures for
decreasing CDAD
3. Describe nursing care of patients with CDAD
in the critical care setting
I
magine that your beloved grandmother has been hospitalized with a
stroke. You are devastated as you
imagine the lifestyle changes that
will shortly ensue. You contemplate
rehabilitation, physical therapy,
and extended care possibilities. Her
progress is good, except for a small
bout of pneumonia that is successfully treated with a course of oral
antibiotics. Therapy resumes, as do
discussions about moving forward.
Then she begins to complain of
abdominal pain, has a mild fever,
and experiences multiple liquid,
Author
Maria E. Pelleschi has more than 20 years of experience as a critical care nurse. Recently a
staff nurse in the cardiovascular surgical intensive care unit at St Vincent Charity Hospital
in Cleveland, Ohio, she is now a nursing instructor at Bryant and Stratton College in
Parma, Ohio.
Corresponding author: Maria E. Pelleschi, RN, MS, CCRN, Bryant & Stratton College, 12955 Snow Rd., Parma, OH
44130 (e-mail: [email protected] or [email protected]).
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].
http://ccn.aacnjournals.org
foul-smelling stools. She has been
placed in isolation, and you don
gloves and gown and lean over to listen as she whispers “I have something called C-diff.”
Clostridium difficile–associated
disease (CDAD) is a confounding
complication. Experienced by patients
in extended care facilities, acute care
areas, and intensive care units, it has
become increasingly prevalent in the
United States since 2003, when
178000 cases were diagnosed.1 The
rate of CDAD is 7 times higher in
persons more than 65 years old than
in persons from 45 to 64 years old.1
Possible explanations for these different rates include greater exposure
to hospitals and extended care facilities, greater use of antimicrobial
drugs, and decreased host defenses
among older persons.2 CDAD has
become so rampant that reporting
infection with C difficile has become
mandatory in Ohio.3 Conservative
estimates suggest that patients with
CDAD incur at least $3669 extra in
hospital costs and spend at least 3.6
CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 27
additional days in the hospital.4 Costs
may exceed $600 million per year in
short-term care facilities alone.1
Nurses must care for patients
with CDAD and are therefore in
position to prevent its spread. In
this article, I provide an overview
of this disease, its mode of transmission, diagnosis, prevention, and current methods of treatment. I also
discuss the nursing care of patients
who have CDAD.
Susceptible host
(one or more risk factors)
Loss of protective normal flora
(antibiotic exposure and/or decreased stomach acidity)
Exposure to C difficile spores
(bedside items, caregiver’s hands)
Ingestion of spores
(transmission via fecal-oral route)
Definition and Description
CDAD is used to describe a constellation of illnesses caused by the
toxins, A and B, produced by the C
difficile bacillus. The illnesses include
diarrhea, pseudomembranous colitis,
toxic megacolon, perforation of the
colon, and, in some instances, sepsis.5
The emergence of a new, more
virulent strain of C difficile partly
explains the recent increase in CDAD.
This new strain, the North American
pulsed-field gel electrophoresis type
I (NAP I) is more virulent and can
produce greater quantities of toxin
A (16 times more) and toxin B (23
times more) than other strains.2,5
Binary toxin, a third toxin, is also
produced by NAP I, although its significance is unknown.5 Researchers6
in Quebec identified use of fluoroquinolones as the most important
risk factor in the development of
this new strain of C difficile. Other
factors associated with diarrhea,
such as predominant use of highrisk antibiotics, reduction in housekeeping staff, increased nursing
workloads, antiquated facilities,
and general changes in hospital
populations (ie, increased number
of immunocompromised, debilitated,
and elderly patients) may also be
contributing factors.7
Proliferation of C difficile bacteria
causes secretion ofa
Toxin A (exotoxin)
Activation of macrophages and mast cells
Fluid secretion and increased
mucosal permeability because of
increased inflammation
Toxin B (cytotoxin)
Increased leukocytes
Increased cytokines
Profound colonic inflammatory response
Possible necrosis of borders of colon with sloughing of cells
Massive fluid secretion into lumen of the colon
Diarrhea results
Focal ulceration (possibly)
Accumulation of purulent and necrotic debris
Formation of pseudomembranes
Figure Development of Clostridium difficile–associated diarrhea2,5,9-12
a NAP I strain also produces binary toxin, which is associated with more severe signs and symptoms
and with increased production of toxins A and B.
Etiology and Transmission of
C difficile Infection
Clostridium difficile is an anaerobic, spore-forming, gram-positive
bacillus.8 The spores are resistant to
many types of disinfectants, heat,
and dryness and may persist for
months on surfaces such as bed
rails, commodes, electronic thermometers, stethoscopes, skin folds,
and the hands of caregivers.2 The
28 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008
spores can cause disease in persons
at high risk for CDAD.
Transmission of C difficile is via
the fecal-oral route (see Figure). In
healthy persons, growth of C difficile
is kept in check by normal flora in
the gut. Possibly, use of antibiotics
and medications that decrease stomach acidity, such as proton pump
inhibitors, cause C difficile bacteria
to proliferate.9
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often mucoid and foul smelling.
Some have described it as having a
characteristic “barnyard” odor.13
Associated signs and symptoms
include nausea, dehydration, and
low-grade fever. Leukocytosis may
occur.5,10
Colitis occurs with severe forms
of the disease and causes profuse
diarrhea and abdominal pain, often
with fever, nausea, abdominal distension, and dehydration. Characteristic raised white and yellow
Table 1 Risk factors for Clostridium difficile–associated disease6,9
Exposure to antimicrobial agents such as clindaymycin, cephalosporins, quinolones,
and penicillin
Gastrointestinal surgery
Advanced age
Presence of a feeding tube
Chemotherapy agents
Environmental exposure
Severe underlying illness
Decreased stomach acidity (H2-blockers or proton pump inhibitors)
Pathophysiology
Once in the colon, C difficile, its
growth unchecked by normal flora
or stomach acid, produces 2 toxins:
an enterotoxin (toxin A) and a more
potent cytotoxin (toxin B).10,11 Toxin
A activates macrophages and mast
cells,11 which release inflammatory
mediators. The mediators cause
disruption of the cell wall junction,
resulting in increased permeability
of the intestinal wall and subsequent diarrhea.5,11 Meanwhile, toxin
B causes degradation of epithelial
cells in the colon.5 As the colitis
worsens, purulent and necrotic
debris accumulates and forms characteristic ulcers, the pseudomembranes11 (see Figure).
cramping in the lower part of the
abdomen without systemic signs
and symptoms.5 The diarrhea is
Table 2 Clinical manifestations and treatment of various severities of Clostridium
difficile–associated disease
Clinical
manifestations5,13
Mild to moderate nonbloody
diarrhea
Cramping in lower part of
abdomen
Vomiting
Dehydration
Fever
Mild abdominal tenderness
Leukocytosis
Treatments and
interventions14-21
Cessation of suspected causative
agent
Administration of metronidazole,
orally or intravenously
Administration of vancomycin,
orally or via nasogastric tube
Contact isolation
Monitoring for dehydration
Fluid replacement as indicated
Frequent skin assessment
Use of moisture barriers and
fecal containment devices
Frequent mouth care
Severe
Colitis
Profuse, watery diarrhea
Abdominal pain
Fever
Nausea
Abdominal distention
Dehydration
Pseudomembrane
All of the above
Use of tolevamer when available
commercially
Administration of corticosteroids
Systemic
Fulminant pseudomembranous
colitis
Systemic complications
including sepsis, volume
depletion, electrolyte
imbalance, hypotension
Peritonitis, paralytic ileus,
and toxic megacolon
(decrease in stool)
Hypoalbuminemia and ascites
Colonic wall thickening, lumen
obliteration, pericolonic fat
stranding present on computed
tomography scans
All of the above
Hemodynamic monitoring
Blood pressure support
Volume replacement
Respiratory support
Administration of vancomycin
enema
Immunoglobulin therapy
Surgery for megacolon
Severity
Mild
Risk Factors
A number of risk factors for
CDAD, including the use of antimicrobials, particularly fluoroquinolones, have been identified6 (Table 1).
Patients who are elderly, have severe
underlying disease, have nasogastric tubes in place, have long hospital stays, or are taking proton pump
inhibitors and histamine receptor
antagonists are at particular risk.9
Clinical Manifestations
CDAD can be mild, severe, or
systemic (Table 2). Mild disease is
characterized by nonbloody diarrhea, occasionally accompanied by
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CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 29
plaques may be visualized during
sigmoidoscopy.5,10 Composed of neutrophils, fibrin, mucin, and cellular
debris, these pseudomembranes
appear on inflamed colonic mucosa
as raised nodules, usually 2 to 10
mm in diameter.22
Complications such as sepsis,
volume depletion, electrolyte
imbalance, hypotension, peritonitis,
paralytic ileus, and toxic megacolon
may be present in systemic CDAD.5
Hypoalbuminemia and ascites may
also be evident.23 A decrease in diarrhea may occur in systemic disease
as a result of toxic megacolon or
paralytic ileus.5,10 Computed tomography scans may show thickening
of the colon wall or obliteration of
the lumen.23 Patients with systemic
disease associated with megacolon
may require surgery.5,10
Diagnosis
Diagnosis of CDAD is based on
signs and symptoms, verification of
the presence of toxins A and B in
stool cultures, and, in many instances,
detection of pseudomembranous
colitis. Pseudomembranous colitis is
verified via colonoscopy. Because of
the risk of perforation and the cost
of this test (mean, $1656 per test),24
experts suggest that colonoscopy be
used with caution, and only for
patients with severe colitis of
unclear origin.10,23
Stool cultures are highly specific
and sensitive for detection of toxin
B; however, they are time intensive
and are not often used.22,23 The
enzyme-linked immunosorbent
assay test for toxin A or toxins A
and B has excellent specificity, and
results are usually available in about
2 hours.22,23 The sensitivity, however,
is only 75% to 85%. Therefore,
cultures of serial stool samples collected on different days are suggested, especially in suspicious cases
in which the initial samples are negative for C difficile.23
The large quantity of stool produced in CDAD allows ample opportunity for specimen collection. Of
note, the toxins themselves are
unstable at room temperature;
therefore, false-negative results may
occur in samples that are not tested
within 2 hours of collection.25 For
that reason, ensuring that stool samples are quickly sent for testing once
obtained is prudent. Because the
stools themselves harbor C difficile
spores, great care must be taken to
avoid contaminating surfaces with
the specimens. Pimetel23 suggests
that specimens be sent and tested
before antibiotic therapy is started
and that contact isolation be initiated on the basis of signs and
symptoms, rather than waiting for
culture results. Sunenshine and
McDonald5 suggest that only watery
or liquid stools be tested. A falsepositive result could indicate that
C difficile colonization is present.
Infection is not likely in persons
who do not have diarrhea.5
Preventing CDAD
Patients treated with antibiotics
must be closely monitored for possible infection with C difficile. Patients
who are elderly, have severe underlying illness, are immunocompromised, or have undergone surgery of
the gastrointestinal tract also require
heightened vigilance.
Prevention of CDAD, however,
entails multidisciplinary efforts to
stem the disease for all patients.
Three elements are required for
prevention of CDAD: proper hand
30 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008
washing, contact isolation, and
environmental measures.
Hand Hygiene
Hands must be washed with an
antimicrobial soap for at least 15
seconds. Although generally beneficial, alcohol-based hand rubs may
not be effective against C difficile
spores.2 A paper towel should be
used to turn off the faucet. Hands
should be washed before and after
contact with a patient and after glove
removal. This technique must be
taught to all of the patient’s family
members as well as the patient.
Reminders to healthcare workers
are also important. In one study,26
effective staff education programs
resulted in a significant reduction in
infection rates. Recommendations
include clustering of nursing care,
hand hygiene education, and ongoing audit and surveillance programs.26
Contact Isolation
Guidelines of the Centers for
Disease Control and Prevention
mandate contact isolation for all
patients with CDAD. Private rooms
are recommended if available; however, if necessary, 2 patients with
CDAD can be placed together. All
persons entering the patient’s room,
including the patient’s family members, must use protective gowns and
gloves. Use of dedicated equipment
such as thermometers and stethoscopes is also recommended.2
Such imposed isolation requires
compassionate yet firm teaching
and support for patients and their
family members. All hospital employees, including physicians, therapists,
clergy, and technicians, must abide
by isolation guidelines, no matter
how brief their visit.
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Environmental Measures
Spores of C difficile tend to
thrive on hospital surfaces. For that
reason, stringent daily cleaning of
all hospital surfaces likely to be contaminated with feces is essential. A
hypochlorite-based disinfectant
that has been registered with the
Environmental Protection Agency
or a 1:10 bleach solution is recommended.2 Frequently touched surfaces such as doorknobs, light
switches, call lights, television remote
control devices, soap dispensers,
faucets, bed rails, and telephones
also require thorough daily cleaning. Hospital policies regarding dedicated equipment, dishes, linens,
waste, and patient transport should
be in place and enforced. Nondisposable equipment such as glucose
meters, cardiac monitors and electrocardiography and x-ray machines
should be disinfected according to
manufacturers’ guidelines.
Nurse managers at a hospital in
England attribute a significant
decrease in C difficile infection to
changes in environmental policies and
replacement of outdated commodes
and mattresses. A decrease in length
of stay and cost savings were also realized as a result of these changes.27
Treatment
The various treatments suggested
for CDAD and their efficacy are matters of much debate. A review of
basic and more recent innovative
treatments follows (Table 3). As
Bartlett14(p429) notes “It can be safely
concluded that all of these treatments
work some of the time, none work
all of the time.” This comment reflects
the confounding nature of CDAD
and the necessity of impeccable
nursing practices.
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Table 3 Treatment options for Clostridium difficile–associated disease (CDAD)14-20,28
Treatment
Metronidazole
Dosing
Comments
500 mg by mouth 3 Oral route preferred
times a day or 500 Less expensive than vancomycin
mg intravenously
every 6 hours
Vancomycin
125 mg by mouth
4 times a day
Nitazoxanide
500 mg by mouth
twice a day
Tolevamer
3-6 g/d by mouth
Oral route preferred, may also be given via
enema or nasogastric tube
Intravenous route not effective for CDAD
May lead to vancomycin resistance
Blocks anaerobic metabolism
Inhibits growth of C difficile in vitro
Nonantibiotic polymer
Not yet available commercially
For mild to moderate CDAD
May cause hypokalemia
Immunoglobulin 300-500 mg/kg
1-6 doses given
Proposed for intractable and severe CDAD
Probiotics
Given orally
Variable dosing
Further studies recommended before
generalization into practice
Donor stool
25 mL given via
nasogastric tube
Meant to replace normal bowel flora
Specific donor criteria
Further studies suggested
Antibiotics
The first treatment for CDAD is
cessation of the suspected causative
antibiotic.23 Although stopping the
antibiotic may be effective, the reason the antibiotic was prescribed in
the first place should be considered,
and monitoring for recurrence or
worsening of the underlying infection is essential.
Oral metronidazole, 250 to 500
mg 4 times a day for 7 to 14 days, is
generally recommended as an initial
treatment.29 Metronidazole can also
be given intravenously.30 Administered by either route, the same dosage
provides bactericidal levels of the
drug in the bowel lumen.
Although equally effective as
metronidazole when given orally,30
vancomycin, standard dosage 1 g/d
for 10 days, is more expensive, and
is therefore reserved for patients
who can not tolerate metronidazole,
are pregnant or breastfeeding, or
have severe cases of CDAD.23,29,30
Alternative vancomycin dosing
strategies may be effective for treatment of recurrent CDAD.31 A pulsed
dosing regimen, intermittent delivery of between 125 and 500 mg
every 3 days, and tapered dosing,
administering the antibiotic over
long periods at decreasing doses,
may in some instances effectively
eradicate vegetative C difficile cells.31
In addition to its greater cost, a
disadvantage of vancomycin is the
occurrence of vancomycin-resistant
strains.23 Intraluminal concentrations of vancomycin cannot be
achieved by intravenous infusion as
they can with metronidazole.30 However, vancomycin can be given via a
nasogastric tube or as an enema.30
Instilling vancomycin as an enema
can be challenging, particularly
when a patient is experiencing diarrhea. This route is suggested as an
adjunct for patients with persistent
CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 31
or severe CDAD, severe ileus, or fulminant colitis.15 The medication can
be given at dosing intervals of 4 to
12 hours, with doses of 2 to 3 g/d,
by using an 18F Foley catheter or a
soft 6F pigtail catheter. The risk of
bowel perforation, inherent any
time an enema is given, mandates
particular vigilance for these patients.
Ideally, the enema should be retained
for 60 minutes. Vancomycin can also
be given via colostomy, ileostomy, or
during colonoscopy.15
Oral rifampin has been given
with metronidazole as an adjunct
therapy. A prospective, randomized,
single-blind study16 of 39 patients
was conducted to compare the efficacy of metronidazole therapy alone
with that of metronidazole plus
rifampin. The researchers could
not demonstrate a therapeutic benefit of this drug combination and
halted their study early, citing
study futility and urging better
treatment protocols.16
More promising results are suggested by a study17 in which oral
metronidazole was compared with
nitazoxanide. A nitrothiazolide,
nitazoxanide works by blocking
anaerobic metabolism and is used to
treat intestinal infections caused by
the protozoa Cryptosporidium and
Giardia. Patients receiving nitazoxanide were given 500 mg every 12
hours for 7 or 10 days. Those receiving metronidazole received 250 mg
every 6 hours for 10 days. For both
groups, the time of resolution of
their signs and symptoms, clinical
response after 7 days of treatment,
and sustained response after 31
days were determined. Initial data
suggest similar effectiveness for
metronidazole and nitazoxanide.
Further studies are being designed
to compare this new medication
with vancomycin.17
Nonantibiotic Polymer
Not yet available commercially,
tolevamer can also be considered
for treating CDAD. A soluble, highmolecular-weight, anionic polymer,
tolevamer works by binding C difficile toxins A and B.18 Suggested for
use with mild to moderately severe
CDAD, tolevamer is given orally 3
times daily for a total of 3 to 6 g per
day. Initial trial results indicted that
the polymer was fairly well tolerated, provided resolution of signs
and symptoms in 67% of patients,
and was associated with a lower
incidence of recurrence than was
vancomycin.18 Resolution of diarrhea
was comparable to that achieved
with vancomycin; however, tolevamer is also associated with an
increased risk of hypokalemia.18
Immunoglobulin
Immunoglobulin has been proposed as a treatment for intractable
and severe cases of CDAD. In one
study,19 patients were given 1 to 6
doses, ranging between 300 and
500 mg/kg. Of 5 patients with
refractory disease, 3 had resolution
of signs and symptoms within 11
days. Although this treatment looks
promising, immunoglobulin is
expensive and in short supply.19
Probiotics
Probiotics are live organisms
meant to treat particular diseases,
including Helicobacter pylori infections, acute gastroenteritis, and
antibiotic-associated diarrhea,
including CDAD. The most commonly used probiotic agents produce lactic acid and are present in
32 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008
normal microflora. Examples
include Saccharomyces boulardii, Lactobacillus acidophilus, and Lactobacillus plantarum.32 Many studies
of probiotics have been done. Sullivan and Nord32 suggest that
although S boulardii was somewhat
effective, particularly in preventing
recurrent CDAD, further studies are
needed. Dendukuri et al20 similarly
determined that evidence was insufficient to recommend the routine
clinical use of probiotics to treat
CDAD in adults.
Corticosteroids
Use of corticosteroids in a child
with refractory CDAD has been
described.33 Typically used for acute
flare-ups of inflammatory bowel
disease, corticosteroids may also be
beneficial in CDAD. Further studies
are needed.
Donor Stool Transplants
A potential means of replacing
normal bowel flora is transplanted
stool. In one study,28 18 patients
were each given 25 mL of donor
stool via a nasogastric tube. Stool
transplant donors were persons
who had not received antimicrobial
therapy for 6 months, had intimate
contact with the patient (ie, spouse
or significant other, family household members), or were otherwise
healthy donors. Two patients in the
study died of unrelated illness;
however, the remaining patients
experienced a 94% cure rate, that is,
reported return of normal bowel
function. Further studies are suggested before donor stool transplants are used routinely.28
Although aesthetic, logistical, and
ethical issues may need to be considered, Aas et al28 contend that the
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patients in the study were receptive
to the prospect of stool transplant.
stools have tremendous needs with
respect to skin integrity and comfort.
Surgery
CDAD that progresses to paralytic ileus, toxic megacolon, or sepsis despite appropriate treatment
may require surgical intervention.21
Fulminant pseudomembranous colitis is typically associated with high
mortality related to hypotension,
acute renal failure, and respiratory
failure. Researchers21 in Canada concluded that total abdominal colectomy performed within 72 hours of
diagnosis of fulminant pseudomembranous colitis improves survival
rates. They21 therefore support early
surgical interventions.
Prevent Dehydration
Prevention of dehydration is
essential for patients with CDAD.
Patients’ weights, fluid intake and
output, and levels of electrolytes,
albumin, and protein must be monitored and corrected as needed.
Intake of protein, iron, and vitamin
C should be encouraged as tolerated.34 Patients should be monitored for clinical manifestations of
dehydration, including rapid,
thready pulse; decreased blood
pressure; diminished peripheral
pulses; flat neck veins; increased
rate and depth of respiration; fever;
decreased level of consciousness;
and decreased urine output with
increased specific gravity. Patients
should also be assessed for the presence of dry flaky skin with poor turgor, thirst, and mouth fissures.34,35
Fluid balance should be restored
through intravenous therapy based
on frequent assessment of vital
signs, urine output, and hemodynamic parameters. When possible,
oral rehydration should be encouraged. Mouth care should be provided frequently, and patients
should be instructed to avoid the
use of lemon-glycerin swabs and
commercial mouthwashes.34,35
Fever, nausea, and dehydration
due to fulminant disease could
result in hypotension, tachycardia,
and hypovolemia.21 Because
antiperistaltic agents such as
diphenoxylate hydrochloride and
atropine sulfate may predispose
patients with CDAD to toxic
megacolon, these drugs are not
recommended.5,11,22 Use of narcotics should also be avoided.5
Nursing Care
CDAD is a complication encountered by patients hospitalized for
other illnesses. Patients, therefore,
must be monitored and treated for
their underlying illness. In addition,
they must be closely monitored for
elevated white blood cell counts,
fever, abdominal pain, and, most
certainly, diarrhea. The goals of care
include prevention of CDAD, early
recognition and treatment of the
disease, promotion of comfort, and
prevention of skin breakdown.
Priorities of Care
All patients with CDAD require
monitoring of vital signs and hemodynamic status. In addition to gastrointestinal assessment, monitoring
of renal, respiratory, and neurological status is imperative in order to
detect and treat systemic manifestations. Aggressive intervention to
treat dehydration and abnormalities
revealed by laboratory tests is essential. Patients with copious liquid
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Promote Comfort
Numerous liquid bowel movements associated with abdominal
tenderness, pain, or cramping are
certainly cause for misery. Mandated
isolation may lead to emotional distress.36 Compassionate measures can
minimize these problems. Therefore,
it is imperative to monitor for pain,
offer analgesia as indicated, provide
frequent skin and mouth care, and
assess for depression or sadness.
Patients’ satisfaction during isolation
can be enhanced by measures that
include providing ongoing communication, estimating duration of isolation, maintaining access to telephone
and television, and promoting the
patient’s sense of control.36
Maintain Skin Integrity
Prevention of skin breakdown is
enormously challenging because of
the frequency, amount, and characteristics of stools in patients with
CDAD. Excessive moisture, alkaline
pH, colonization with microorganisms, and friction contribute to skin
breakdown.37 Goals of perineal skin
care include regularly removing skin
irritants, minimizing exposure to
bacteria, and establishing a healing
local environment. Cleansers that
contain water and surfactants, are
near the normal skin pH of 5.5, and
provide moisture should be selected.
The perineum should be cleansed
daily and with each bowel movement. Creams or ointments that
serve as moisture barriers should be
applied after cleaning.37 A possible
complication of fecal incontinence is
perineal dermatitis. A recent study38
indicated the need for staff compliance and consistency in the use of
products and measures in the prevention of this complication.
CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 33
Table 4 Summary of nursing plan of care34-39
Situation
Risk for deficient fluid volume
related to Clostridium
difficile–associated disease
Nursing care
Monitor vital signs, fluid status, and
hemodynamic parameters closely
Encourage adequate oral intake as tolerated
Replace fluids and electrolytes as indicated
Alteration in comfort related to
diarrhea and abdominal pain
Monitor for pain
Provide analgesia and comfort measures as
required
Provide frequent mouth and skin care
Risk for loneliness related to
imposed isolation
Assess for depression and sadness
Help patient identify and express feelings
associated with isolation experience
Encourage socialization with family and
significant others as able
Allow patient to maintain access to telephone
and television
Risk for perineal skin
breakdown related to
frequent stools
Keep skin clean and dry after bowel movements
Provide moisture barriers
Protect bony prominences
Use commercial fecal containment system
when indicated; follow manufacturer’s
guidelines closely
Turn and reposition patient every 2 hours as
tolerated
Monitor nutrition status, including albumin
and protein levels, and provide adequate
intake of calories
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Use of commercial fecal diversion
and containment systems may also
be considered. Products such as the
Flexi-Seal fecal management system
(Convatec, Princeton, New Jersey)
contain a silicone catheter with a
retention balloon and a collection
bag.39 The catheter is inserted into
the rectum, and when used properly,
can contain and divert liquid or
semiliquid stool away from the perineum. Manufacturer guidelines
should be followed closely, especially
with respect to the length of time
this treatment may be continued,
recommended balloon pressure,39
and before instilling medications.
critical care nurses to provide early
and thorough assessment of those
most at risk. Impeccable nursing
care must be provided to those with
CDAD (Table 4). In the 1800s, Florence Nightingale wrote, “It may
seem a strange principle to enunciate as the very first requirement in a
hospital that it should do the sick no
harm.” Prevention is the most
important treatment.
Financial Disclosures
None reported.
13.
14.
15.
16.
17.
References
Conclusion
The possibility that CDAD may
develop in our patients challenges
34 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008
1. McDonald LC, Owings M, Jerigan DB.
Clostridium difficile infection in patients discharged from US short-stay hospitals, 19962003. Emerg Infect Dis. 2006;12(3):409-415.
http://www.cdc.gov/ncidod/EID/vol12no03
/05-1064.htm. Accessed November 26, 2007.
2. Centers for Disease Control and Prevention.
Clostridium difficile information for healthcare providers: FAQ: CDC infection control.
2005. http://www.cdc.gov/ncidod/dhqp
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/id_CdiffFAQ_HCP.html. Accessed November 26, 2007.
Ohio Department of Health. Clostridium
difficile. 2006. http://www.odh.state.oh.us
/pdf/idcm/clostdif.pdf#search=
%22incidence%20CDAD%20Ohio
%20Department%20of%20health%22.
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Kyne L, Hamel MB, Polavaram R, et al.
Health care costs and mortality associated
with nosocomial diarrhea due to Clostridium
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Sunenshine RH, McDonald LC. Clostridium
difficile-associated disease: new challenges
from an established pathogen. Cleve Clin J
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Pepin J, Saheb N, Coulombe MA, et al.
Emergence of floroquinolones as the predominant risk factor for Clostridium
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during an epidemic in Quebec. Clin Infect
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Loo VG, Libman MD, Miller MA, et al.
Clostridium difficile: a formidable foe. CMAJ.
2006;171(1):47-48.
Murray PR, Rosenthal KS, Pfaller AM. Medical Microbiology. 5th ed. Philadelphia, PA:
Elsevier Mosby; 2005:411-413.
Dial S, Alrasadi K, Manoukian C, Huang A,
et al. Risk of Clostridium difficile diarrhea
among inpatients prescribed proton pump
inhibitors: cohort and case-control studies.
CMAJ. 2004;171(1):33-38.
Poutanen SM, Simor AE. Clostridium difficile-associated diarrhea in adults. CMAJ.
2004;171(1):51-58.
Schroeder MS. Clostridium difficile-associated
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/921.pdf. Accessed November 26, 2007.
Perloff S, Horn D. Community-acquired
Clostridium difficile colitis. Emerg Med.
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.com/html/pre/fea/features/039070037.asp.
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Grainger M. A staff nurse’s perspective of
infection control problems. Br J Nurs. 2005;
14(17):912-916.
Bartlett JG. New drugs for Clostridium difficile infection. Clin Infect Dis. 2006;43(4):
428-431.
Apisarnthanarak A, Mundy LM. Intracolonic vancomycin for adjunctive treatment of severe Clostridium difficile colitis:
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Lagrotteria D, Holmes S, Smieja M, Smaill
F, Lee C. Prospective, randomized inpatient
study of oral metronidazole versus oral
metronidazole and rifampin for treatment
of primary episodes of Clostridium difficileassociated diarrhea. Clin Infect Dis. 2006;
43(5):547-552.
Musher DM, Logan N, Hamill RJ, et al.
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43(4):421-427.
Louie TJ, Peppe J, Watt CK, et al. Tolevamer,
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Wilcox MH. Descriptive study of intravenous immunoglobulin for the treatment
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20. Dendukuri N, Costa V, McGregor M, et al. Probiotic therapy for the
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http://ccn.aacnjournals.org
CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 35
CE Test Test ID C0813: Clostridium dif f icile–Associated Disease: Diagnosis, Prevention, Treatment, and Nursing Care
Learning objectives: 1. Discuss the incidence of Clostridium difficile-associated disease (CDAD) in the critical care setting 2. Identify key preventive measures
for decreasing CDAD 3. Describe nursing care of patients with CDAD in the critical care setting
1. The incidence of Clostridium difficile–associated disease (CDAD) is higher
in which age group?
a. 45 to 55 years
b. 30 to 65 years
c. < 30 years and immune compromised
d. > 65 years
2. Which of the following states have mandated reporting of C difficile?
a. New Hampshire
b. Ohio
c. Florida
d. Arizona
3. Recent increases in CDAD have been associated with the emergence of
which new strain?
a. North American virulent mucoid strain
b. Northern Canadian pulse field-electrophoresis type I
c. North American pulse-field gel electrophoresis type I
d. North American pulse-field
4. Which of the following is an identified risk factor for C difficile?
a. Retention urinary catheters
b. Short hospital stays
c. Surgical procedures
d. Use of proton pump inhibitors and histamine receptor antagonists
7. Which of the following best describes 3 elements for preventing CDAD?
a. Wearing personal protective equipment, spraying sanitizer on surfaces,
and proper hand washing
b. Using alcohol-based hand sanitizers, reverse isolation, and wearing proper
personal protective equipment
c. Cooking meat to proper temperature, proper hand washing, and limiting
use of histamine receptor antagonist
d. Proper hand washing, contact isolation, and environmental measures
8. All persons entering a room with CDAD, no matter the duration of
their visit, must wear which of the following?
a. Gloves, booties, and mask
b. Gloves and mask
c. Full isolation suit
d. Protective gown and gloves
9. What cleaning solution is recommended for disinfecting surfaced likely
to be contaminated with C difficile?
a. 1:5 bleach solution
b. 1:20 bleach solution
c. 1:10 bleach solution
d. None of the above
10. Which antibiotic is recommended as the initial treatment for CDAD?
a. Metronidazole, 250 to 500 mg 4 times daily for 7 to 14 days
b. Fluconazole, 200 to 400 mg daily for 7 days
c. Ketoconazole, 200 to 400 mg daily for 7 days
d. Loperamide, 2 mg after each loose stool
5. Which of the following is not a systemic complication of CDAD?
a. Hyperbilirubinemia
b. Sepsis
c. Hypovolemia
d. Peritonitis
6. False negative results for C difficile may occur if samples are not tested
within how many hours of collection?
a. 8 hours
b. 6 hours
c. 2 hours
d. 12 hours
11. Which of the following best describes nursing care of patients
diagnosed with CDAD?
a. Monitoring vital signs
b. Monitoring renal status
c. Aggressive interventions to prevent dehydration
d. All of the above
12. Measures to enhance patient satisfaction for those in mandatory
isolation include all except which of the following?
a. Limiting visitations from family and friends
b. Providing ongoing communica tion
c. Estimating duration of isolation
d. Maintaining access telephone and television
Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. K a
Kb
Kc
Kd
2. K a
Kb
Kc
Kd
3. K a
Kb
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4. K a
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5. K a
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6. K a
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7. K a
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8. K a
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9. K a
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11. K a
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10. K a
Kb
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12. K a
Kb
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Test ID: C0813 Form expires: February 1, 2010 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Category: A, Synergy
CERP A Test writer: Todd M. Grivetti, RN, BSN, CCRN
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