Download A Descriptive Study Oral Health Status and Development of

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
Oral Health Status and Development of Ventilator-Associated Pneumonia:
A Descriptive Study
C indy L. M unro, M ary Jo G rap, R .K. E lswick, Jr, Je ssica M cKinne y, C urtis N . S e ssle r a nd R usse ll S .
H um m el, III
Am J C rit C are. 2006;15: 453-460
© 200 6 Am e rica n Associa tion of C ritica l-C a re N urse s
P ublishe d online http://www.a jcconline .org
P ersona l use only. F or copyright pe rm ission inform a tion:
http://a jcc.a a cnjourna ls.org/cgi/e xte rna l_ re f?link_ type = P E R M IS S IO N D IR E C T
Subscription information
http://ajcc.aacnjournals.org/subscriptions
Information for authors
http://ajcc.aacnjournals.org/m isc/ifora.shtm l
Submit a manuscript
http://www.editorialm anager.com /ajcc
Email alerts
http://ajcc.aacnjournals.org/subscriptions/etoc.shtm l
AJC C , the Am erican Journal of C ritical C are, is the official peer-reviewed research
journal of the Am erican Association of C ritical-C are N urses (AAC N ), published
bim onthly by T he InnoV ision G roup, 101 C olum bia, Aliso V iejo, C A 92656.
T elephone: (800) 899-1712, (949) 362-2050, ext. 532. F ax: (949) 362-2049.
C opyright © 2006 by AAC N . All rights reserved.
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
ORAL HEALTH STATUS AND DEVELOPMENT OF VENTILATORASSOCIATED PNEUMONIA: A DESCRIPTIVE STUDY
By Cindy L. Munro, RN, PhD, ANP, Mary Jo Grap, RN, PhD, ACNP, R.K. Elswick, Jr, PhD, Jessica McKinney, BS,
Curtis N. Sessler, MD, and Russell S. Hummel III, BS, MS. From Adult Health Department, School of Nursing
(CLM, MJG, RKE), Department of Biostatistics (RKE, JM), Division of Pulmonary and Critical Care Medicine,
Department of Internal Medicine (CNS), and Department of Surgery (RSH), School of Medicine, Virginia
Commonwealth University, Richmond, Va.
• BACKGROUND Ventilator-associated pneumonia is a significant cause of morbidity and mortality and
may be influenced by oral health.
• OBJECTIVE To describe the relationship between ventilator-associated pneumonia and oral health status,
changes in oral health status during the first 7 days after intubation, and microbial colonization of the
oropharynx and trachea.
• METHODS A total of 66 patients were enrolled within 24 hours of intubation and were followed up for
up to 7 days. Data on oral health measures and the Clinical Pulmonary Infection Score (CPIS) were collected at baseline, day 4 (n = 37), and day 7 (n = 21). A regression model was used to predict risk of
pneumonia at day 4.
• RESULTS Dental plaque and oral organisms increased over time. Correlations were significant for
baseline and day 4 dental plaque (P < .001), baseline salivary lactoferrin and day 4 plaque (P = .01),
and lower salivary volume and higher day 4 CPIS (P = .02). Potential pathogens were identified in oral
cultures for 6 patients before or at the same time as the appearance of the organisms in tracheal aspirates. Correlations were significant with day 4 CPIS for score on the Acute Physiology and Chronic
Health Evaluation (APACHE) II (P = .007), day 4 salivary volume (P = .02), interaction of APACHE II
score and day 1 CPIS (P < .001), and interaction of day 1 CPIS and plaque (P = .01).
• CONCLUSIONS Higher dental plaque scores confer greater risk for ventilator-associated pneumonia,
particularly for patients with greater severity of illness. Salivary volume and lactoferrin may affect the
risk. (American Journal of Critical Care. 2006;15:453-460)
V
entilator-associated pneumonia (VAP) is
defined as pneumonia in a patient receiving
mechanical ventilation that was neither present nor developing at the time of intubation. VAP
increases mortality,1 length of stay,2,3 and cost.2,4,5 Oral
Corresponding author: Cindy L. Munro, RN, PhD, ANP, Professor, School of Nursing,
Virginia Commonwealth University, Box 980567, Richmond, VA 23298-0567
(e-mail: [email protected]).
To purchase electronic or print reprints, contact The InnoVision Group, 101
Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050
(ext 532); fax, (949) 362-2049; e-mail, [email protected].
http://ajcc.aacnjournals.org
health status can be compromised by critical illness
and by mechanical ventilation and is influenced by
nursing care.6,7 However, the extent of oral changes in
critically ill patients and the relationship between oral
health status and development of VAP have not been
extensively studied.
A major risk factor for VAP is colonization of
the oropharynx by potential pathogens such as
Staphylococcus aureus, Streptococcus pneumoniae,
and gram-negative rods.8-11 Several factors contribute
to the importance of oral health status in the development of VAP.
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
453
Within 48 hours of admission to the intensive care
unit (ICU), patients have changes in oral flora to predominantly gram-negative organisms, which include
more virulent organisms.12,13 Dental plaque can provide an environment for microorganisms that cause
VAP, and dental plaque of patients in the ICU can be
colonized by potential respiratory pathogens such as
methicillin-resistant S aureus and Pseudomonas aeruginosa.14 In addition, abnormalities in salivary flow may
place patients at risk for overgrowth of organisms in
the oropharynx. Circulation of saliva in the mouth
provides mechanical removal of debris and plaque,
and saliva contains both innate and specific immune
components active in controlling oral microorganisms.15-18 Thus, salivary volume and amounts of salivary immune components such as lactoferrin and
immunoglobulin A may influence oropharyngeal colonization and development of VAP. Tubes traversing the
oral cavity that keep the mouth open may contribute to
the accumulation of dental plaque by exacerbating
xerostomia (dry mouth). Many medications also reduce
salivary flow.
The bacteria found in dental plaque may
cause ventilator-associated pneumonia.
Oral health status in critically ill adults is an important issue, but it has not been well studied. The specific
aim of this study was to describe the relationship
between oral health status and the development of VAP.
Specifically, we examined the relationship between oral
health status, as indicated by assessment of the oral
cavity, cultures of oral specimens, salivary volume, and
salivary immune components, and development of
VAP, as indicated by the Clinical Pulmonary Infection
Score (CPIS). In addition, we determined changes in
oral health status during the first 7 days of intubation
and mechanical ventilation and the relationships
between microbial colonization of the oropharynx and
colonization of the trachea over time.
Methods
Design and Sample
A nonexperimental, longitudinal, descriptive design
was used. The study was approved by the Virginia
Commonwealth University Office of Research Subjects Protection and was carried out in accordance
with the ethical standards set forth in the Helsinki
Declaration of 1975. Subjects were recruited from the
454
medical respiratory ICU at Virginia Commonwealth
University Health Systems in Richmond, Va. This 12-bed
unit has about 1000 admissions each year; approximately 50% of the patients admitted require mechanical ventilation.
All patients admitted to the unit were reviewed for
potential enrollment in the study. Patients receiving
mechanical ventilation were enrolled within 24 hours
of intubation. Because reintubation increases the risk
for VAP,19,20 patients who already had had endotracheal
intubation during the current hospital admission were
excluded. Data were obtained during a period of up to
7 days or until extubation. Because clinical evidence
of VAP occurs after 48 hours of intubation, data on
VAP and oral health were collected on days 1 (baseline), 4, and 7.
Measurement and Quantification of Key Variables
Oral Health Status. Evaluation of oral health status had 5 components:
1. a baseline count of decayed, missing, and filled
teeth;
2. an assessment of the oral cavity;
3. a culture of an oral specimen;
4. measurement of salivary volume; and
5. analysis of 2 salivary immune components:
immunoglobulin A and lactoferrin.
Assessment of the oral cavity consisted of visually
scoring 9 components:
1. dental plaque,
2. inflammation,
3. bleeding,
4. purulence,
5. candidiasis,
6. calculus,
7. stain,
8. caries, and
9. salivary flow (observed salivary volume).
The assessments were documented by using a 100mm visual analog scale (VAS) for each component.
These components were chosen on the basis of previous work21,22 and were developed in conjunction with a
dental hygiene faculty member and a biostatistician.
Salivary flow determined by using the VAS was
significantly correlated with the objective measurement of salivary volume (r = 0.70; P = .006). Number
of teeth decayed was significantly correlated with
VAS caries (r = 0.83; P < .001). In addition, VAS items
not expected to change over time were highly correlated on different days (caries, r = 0.90, P < .001; stain,
r = 0.94, P < .001). This assessment tool provided
greater discrimination than categorical scoring systems do; data collectors were extensively trained and
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
http://ajcc.aacnjournals.org
were periodically retested to maintain interrater reliabilities greater than 0.90.
Cultures of oral specimens were evaluated microscopically (Gram stain) and semiquantitatively. Each culture was scored on a 3-point scale identical to the CPIS
scale used to describe cultures of tracheal aspirates:
1 = no growth or few bacteria,
2 = moderate or large number of bacteria, and
3 = large number of bacteria and same bacteria
seen on Gram stain.
Several other risk factors may contribute to the
development of VAP. Descriptive data related to these
risk factors also were collected, including demographics and severity of illness as determined by scores on
the Acute Physiology and Chronic Health Evaluation
(APACHE) II. Demographic data included sex, race,
age, previous use of antibiotics, reason for intubation,
type of intubation, intubation process, and reason for
admission to the ICU.
Procedure
Oral comfort care did not affect
pneumonia risk.
After the oral assessment, a sample of saliva was
collected from the sublingual pocket on the dependent
side of the mouth by means of a salivette (Sarstedt
Inc, Newton, NC). The salivette was centrifuged to
recover the saliva, and the volume of the recovered
saliva was measured. Levels of salivary immunoglobulin A and lactoferrin were determined by using an
enzyme-linked immunosorbent assay (R&D Systems,
Minneapolis, Minn). Aliquots of saliva samples were
stored at -70ºC until assay. All assays were performed
in triplicate.
Ventilator-Associated Pneumonia. Development
of VAP was determined by using the CPIS.23-25 With
the CPIS, points are assigned to 6 easily obtained variables:
1. body temperature,
2. white blood cell count,
3. tracheal secretions,
4.oxygenation (ratio of PaO2 to fraction of inspired
oxygen),
5. f indings on chest radiograph (radiologist’s
report), and
6. cultures of tracheal aspirates (microscopic examination and semiquantitative culture of tracheal secretions, scored by using the same scale as for the oral
cultures).
Points for each variable of the CPIS are summed,
yielding a total CPIS (range 0-12), which provides a
range of scores for data analysis. Although some
investigators26,27 have used the CPIS as a dichotomous
measure of VAP (CPIS = 6 indicates pneumonia, and
CPIS <6 indicates no pneumonia), other investigators 12,23,28 have used the entire range of scores to
describe the clinical development and progression of
pulmonary infection over time. We used the full range
of scores to describe the risk of VAP.
http://ajcc.aacnjournals.org
For each patient, if inclusion criteria were met, the
study was explained to the patient’s legally authorized
representative and consent was obtained. Data were
collected from time of enrollment in the study through
day 7 of intubation or until extubation. Oral health status and CPIS were determined 3 times during the
study: within 24 hours of intubation (baseline, at time
of enrollment), at 72 to 96 hours after intubation (during day 4 of intubation, corresponding to the definition of early-onset VAP29), and at 144 to 168 hours
after intubation (during day 7 of intubation, corresponding to late-onset VAP29). Data related to other
risk factors for VAP were collected daily and included
information on ventilator support, enteral nutrition,
and selected medications.
As salivary volume decreased, risk of
pneumonia increased.
Data Analysis
Descriptive statistics were used to summarize the
characteristics of the study population; percentages
were calculated for discrete variables and means and
SDs for continuous variables. A general forward
selection multiple regression analysis was used to
model the relationship between oral health status and
CPIS at day 4. Day 4 was chosen because the sample
size at day 7 was small because of loss of patients
(extubation or death). Variables examined included
baseline CPIS, oral assessment scores, salivary volume, salivary immunoglobulin A, salivary lactoferrin,
and demographic variables. The final model had the
highest overall analysis of variance F ratio (F6,21 = 4.86,
P = .006) and adjusted R2 (R2adj = 0.52). Model parameters are presented in Table 1. Finally, model assumptions were checked by examining the residual by
predicted plot, the normal quantile plot of the residuals, and regression diagnostics.
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
455
Table 1 Model parameter estimates
Table 2 Characteristics of the sample
Estimate
(SE)
t ratio
P
APACHE
0.172 (0.055)
3.14
.007*
Salivary volume
-0.002 (0.001)
-2.61
.02†
CPIS1
-0.098 (0.202)
-0.49
.63
Score on Acute Physiology
and Chronic Health
Evaluation II
Plaque
0.005 (0.017)
0.28
.79
No. of decayed teeth
1.08
0-7
No. of missing teeth
13.85
0-36
No. of filled teeth
0.82
0-9
Total No. of decayed, missing,
and filled teeth
15.75
0-36
Oral care, No. of times per
day
2.58
0-7
Parameter
CPIS1 × APACHE
-0.165 (0.0325)
-5.06
<.001*
CPIS1 × Plaque
-0.034 (0.012)
-2.76
.01†
* Significant at P < .01.
† Significant at P < .05.
Abbreviations: APACHE, Acute Physiology and Chronic Health
Evaluation; CPIS, Clinical Pulmonary Infection Score.
Results
Characteristics of the Sample
The characteristics of the sample are summarized
in Table 2. The 66 patients (mean age 55 years, 58%
men) were ethnically diverse: 59% black, 35% white,
3% Asian, and 1.5% Hispanic. Patients remained in
the study for a mean of 4.2 days. A total of 37 patients
(56%) remained in the study through day 4; 21 (32%),
through day 7. Because patients remained in the study
only while intubated and receiving mechanical ventilation, an important reason for attrition was extubation;
death related to critical illness was another source of
attrition. Most of the patients (65%) were intubated
because of respiratory failure; the remainder were
intubated to provide airway control.
Baseline counts of decayed, missing, and filled
teeth (Table 2) indicated that many patients had oral
health problems before admission. Interestingly, the
number of times per day that oral comfort care was
Variable
Age, y
Mean
Range
55
25-93
20.35
4-41
given did not affect day 4 CPIS (P = .81) and did not
differ significantly between patients in whom VAP
developed and those in whom it did not.
The risk of VAP as evidenced by mean CPIS consistently increased over time (Table 3). Of the 31
patients with complete data through day 4, a total of 8
(26%) had a score of 6 or higher on the CPIS.
Relationship Between Oral Health Status and VAP
Factors significantly related to day 4 CPIS were
APACHE II scores (P = .007), day 4 salivary volume (P
= .02), interaction between baseline CPIS and APACHE
II (P < .001), and interaction between baseline CPIS and
plaque (P = .01). An inverse relationship was observed
between salivary volume and day 4 CPIS; as salivary
volume decreased, CPIS increased. Because our model
has 2 interaction terms (baseline CPIS × APACHE II
and baseline CPIS × plaque), the effect of plaque on
day 4 CPIS could not be directly interpreted.
Table 3 Clinical Pulmonary Infection Score (CPIS) and oral health status variables by study day
Variable
Baseline
Mean (SD)
Day 4
Mean (SD)
Day 7
Mean (SD)
CPIS
3.66 (1.74)
4.26 (2.02)
4.50 (1.79)
Score on visual analog scale for
oral assessment (millimeters
from zero anchor)
Plaque
Salivary flow
21.27 (23.66)
31.86 (28.12)
22.72 (20.47)
31.53 (30.95)
24.32 (29.01)
26.79 (24.10)
Measured salivary volume, µL
357.2 (483.4)
305.9 (448.4)
133.5 (286.9)*
3.5 (4.9)
2.6 (5.8)
3.0 (7.3)
398.5 (155.2)
992.5 (181.4)
535.2 (111.0)
Immunoglobulin A, g/L
Lactoferrin, µg/mL
* Significant at P < .01.
456
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
http://ajcc.aacnjournals.org
28
26
26
26
24
22
20
APACHE II score
28
APACHE II score
APACHE II score
28
24
22
20
18
2.0
3.0
4.0 4.5
22
20
18
1.0
24
18
1.0
2.0
3.0
4.0 4.5
1.0
2.0
3.0
4.0 4.5
CPIS1
CPIS1
CPIS1
Lowest
(cleanest teeth)
Middle
Highest
(most plaque)
Baseline plaque category
0
1
2
3
Predicted CPIS
4
5
6
7
>7
Figure 1 Effect of low (left panel), moderate (middle panel), and high (right panel) amounts of plaque on day 4 Clinical Pulmonary Infection Score (CPIS) across a range of Acute Physiology and Chronic Health Evaluation (APACHE) II scores for
baseline CPIS <5 (indicating pneumonia was not present at baseline). The contour plots are color keyed such that color wavelength is associated with day 4 CPIS (larger wavelength indicates higher CPIS); yellow, orange, and red areas correspond to day
CPIS scores ≥ 6 (indicating pneumonia).
The complex relationship between day 4 CPIS and
plaque, APACHE II scores, and baseline CPIS was
evaluated by using contour plots. In order to generate
the plots, plaque scores were collapsed into 3 categories: low (cleanest teeth), moderate, and high (most
plaque). Figure 1 shows the relationship of these categories to day 4 CPIS across a range of APACHE II
scores for patients who did not have pneumonia at baseline (CPIS <5). The contour plots are keyed so that the
darkest areas correspond to a day 4 CPIS of 6 or greater
(indicating pneumonia). CPIS on day 4 increased as the
APACHE II score increased.
In the most critically ill, increases in
dental plaque increased the risk of
pneumonia.
In patients with the cleanest teeth (Figure 1, left
panel), higher baseline CPIS was predictive of a slight
decrease in day 4 CPIS for patients whose APACHE II
scores were greater than 26. However, for patients
whose APACHE II scores were less than 26, increases
in baseline CPIS were predictive of increased day 4
CPIS. Similar patterns held for patients with moderate
http://ajcc.aacnjournals.org
plaque (Figure 1, middle panel) and the most plaque
(Figure 1, right panel), although the breakpoint for
APACHE II score was 23 in the patients with moderate
plaque and 21 in the patients with the most plaque.
In all categories, when APACHE II and baseline
CPIS were held constant, plaque increases were associated with increased day 4 CPIS. The model indicates
that increased plaque was most predictive of pneumonia in patients with high APACHE scores and lower
baseline CPIS.
Changes in Oral Health Status
During the First 7 Days of Intubation
Data related to oral health status on study days 1
(baseline), 4, and 7 are presented in Tables 3 and 4. Salivary volume decreased over time, with significant differences between day 1 and day 7 (t test, P = .003).
Dental plaque consistently increased over time, although
the differences were not significant. Baseline plaque
score was highly correlated with day 4 plaque score
(r = 0.65, P < .001). Baseline salivary lactoferrin was
positively correlated with day 4 plaque score (P = .01).
Other correlations were not significant.
Temporal Relationships in Microbial Colonization
We examined both the concordance between and
timing of oral and tracheal colonization. The number
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
457
Table 4 Correlations of oral immune variables
Variable
By Variable
Correlation
P
Day 4 plaque
Baseline plaque
0.65
<.001*
Day 4 plaque
Baseline lactoferrin
0.45
.01†
Baseline immunoglobulin A
Baseline lactoferrin
-0.13
.36
Day 4 immunoglobulin A
Day 4 lactoferrin
-0.16
.51
Day 4 plaque
Baseline immunoglobulin A
0.26
.18
Day 4 lactoferrin
Baseline lactoferrin
0.33
.10
Day 4 Clinical Pulmonary Infection Score
Baseline lactoferrin
-0.29
.15
Day 4 Clinical Pulmonary Infection Score
Baseline immunoglobulin A
-0.06
.70
* Significant at P < .01.
† Significant at P < .05.
of organisms present in cultures of oral specimens
increased from day 1 to day 4 and remained high on day
7 (Figure 2). Potential pathogens were detected in the
cultures: S aureus in 4 patients, P aeruginosa in 1
patient, and Acinetobacter baumanii in 1 patient. Importantly, in each instance, the organism was present in oral
cultures on the same sampling day or before the appearance of the organism in cultures of tracheal aspirates.
We tested the agreement between oral culture
scores and tracheal aspirate scores by using a weighted
κ statistic. The analysis revealed significant agreement
on all 3 study days between oral swab score and tracheal aspirate score (day 1, P = .02; day 4, P < .001;
day 7, P = .008).
Discussion
VAP is associated with increased healthcare costs,
morbidity, and mortality. Several factors increase the
risk for VAP. Although strong data link certain risk factors to VAP, the influence of oral health status has not
been examined extensively. We found that the oral health
of critically ill patients is often compromised at the time
of admission and deteriorates over time, and that a relationship exists between oral health status and VAP.
The study sample was a diverse group, with African
Americans and women well represented. Severity of
illness was appropriate for a large urban medical center, and the VAP rate was similar to the rate reported
in the literature.30 Interestingly, the number of decayed,
missing, and filled teeth in our sample is similar to that
reported by Fourrier et al31 (mean 6, SD 8) in a sample
of patients in Europe.
Others have examined dental plaque in ICU patients,
but we focused exclusively on patients receiving
mechanical ventilation, restricted the study to the first 7
days of intubation, and included oral health status
Percentage of cultures
scored as 2 or 3
60
50
40
30
20
10
0
Oral
Tracheal
Day 1
Score = 2
Score = 3
Oral day 4
Tracheal day 4
Oral day 7
Day 4
Tracheal day 7
Day 7
Study day
Figure 2 Oral and tracheal specimens for culture were obtained on study days 1, 4, and 7 and were semiquantitatively scored
on a 3-point scale. Columns represent the percentages of oral and tracheal cultures scored 2 and 3.
458
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
http://ajcc.aacnjournals.org
parameters other than plaque. In a study by Scannapieco
et al,14 a total of 34 patients in a medical respiratory ICU
had mean plaque scores significantly greater than those
of outpatients in a preventive dentistry clinic. Fourrier
et al31 found an increase over time in dental plaque on
premolar teeth in 15 ICU patients examined on study
days 0 and 5. El-Solh et al32 examined dental plaque in
49 elderly long-term care residents at the time of
admission to the ICU and found that dental plaque
was worse in those who were subsequently colonized
with respiratory pathogens than in those who were not
colonized. Scannapieco et al14 did not examine the
relationships between VAP and dental plaque and oral
colonization. Fourrier et al31 found that colonization of
dental plaque with potential pathogens was significantly associated with subsequent nosocomial infections (not limited to VAP).
Good salivary flow enhances the
removal of oral organisms, reducing
pneumonia.
Our data support a link between increases in dental plaque and the development of VAP. The relationship was not straightforward but was influenced by
interactions among dental plaque, baseline severity of
illness, and baseline pulmonary infection status. The
effect of increased plaque was most predictive of pneumonia in patients with high APACHE scores and lower
baseline CPIS. The effect of oral care interventions on
VAP has not been shown, but as plaque-reduction
interventions are tested, patients who have the highest
severity of illness but do not yet have signs of pulmonary infection might derive the most benefit. The
differential benefits of plaque reduction in particular
subgroups of patients require additional investigation.
Association of plaque scores and risk for VAP may
be due to the potential for dental plaque to harbor
pathogens responsible for VAP in the microbially rich
biofilm. Scannapieco et al,14 Fourrier et al,31 and El-Solh
et al32 all found potential VAP pathogens, including S
aureus and P aeruginosa, in the oral cavities of ICU
patients. We also cultured these organisms from oral and
tracheal secretions. Potential pathogens were present in
oral specimens at the same time as or before the appearance of the pathogens in tracheal secretions, similar to
the findings in elderly subjects reported by El-Solh et al.32
We observed that lower baseline salivary volumes
were associated with increased day 4 CPIS (and risk
http://ajcc.aacnjournals.org
of VAP). Because of the importance of salivary flow
in mechanical removal of oral organisms and in distribution of salivary immune components throughout the
oral cavity,15-18 this finding was not surprising. Although
our examination was restricted to the first 7 days of
ventilation, the reduction in salivary volume over time
might contribute to increases in risk for VAP beyond
the period we studied. Many of the medications given
to critically ill patients (including benzodiazepines,
haloperidol, and meperidine) can affect salivary volume. Methods of increasing oral mucosal hydration
merit investigation.
Our data further indicate that levels of innate and
specific immune components in the mouth, particularly
salivary lactoferrin and immunoglobulin A, do change
during critical illness. The role of salivary immune factors has not been thoroughly investigated and might
provide additional insights into risk factors for VAP.
We developed an oral VAS to address difficulties
with previous bedside oral evaluation tools. Our assessment tool has tested reliability and validity, includes
multiple parameters of oral health status, and is designed
to evaluate those parameters as continuous measures.
Some of the individual items on the VAS (eg, caries)
are not expected to change during hospitalization; these
items provide a mechanism for ongoing evaluation of
interrater reliability in individual patients or groups of
patients. Of note, we were able to maintain a greater
than 0.90 interrater reliability throughout the study with
minimal training.
Dental plaque and salivary volume can be determined by bedside clinicians and are associated with
risk for VAP. These factors are theoretically amenable
to alteration by nursing interventions, although oral
care interventions in adults receiving mechanical ventilation have not been tested extensively. However, current oral care is focused on comfort rather on plaque
removal or stimulation of salivary flow. We are testing
the effect of specific oral care interventions on removal
of plaque and reduction of the incidence of VAP in
patients in a surgical, medical, and neuroscience ICU.
Optimal oral care should focus on
plaque removal and stimulation of
salivary flow.
Oral care interventions that prevent the accumulation of plaque and stimulate local oral immunity during the early period of hospitalization might reduce
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
459
development of VAP. These relationships require further examination and might guide the development
of effective nursing care interventions for prevention
of VAP.
ACKNOWLEDGMENTS
This research was supported by grants from the National Institute of Nursing
Research (R15 NR07730 to MJG) and the A.D. Williams Foundation, Virginia
Commonwealth University (to CLM).
REFERENCES
1. Cook D. Ventilator associated pneumonia: perspectives on the burden of
illness. Intensive Care Med. 2000;26(suppl 1):S31-S37.
2. Byers JF, Sole ML. Analysis of factors related to the development of ventilator-associated pneumonia: use of existing databases. Am J Crit Care.
2000;9:344-349.
3. Rodriguez JL, Gibbons KJ, Bitzer LG, Dechert RE, Steinberg SM, Flint
LM. Pneumonia: incidence, risk factors, and outcome in injured patients.
J Trauma. 1991;31:907-912.
4. Leu HS, Kaiser DL, Mori M, Woolson RF, Wenzel RP. Hospital-acquired
pneumonia: attributable mortality and morbidity. Am J Epidemiol. 1989;
129:1258-1267.
5. Haley RW, Schaberg DR, Crossley K, Von Allmen SD, McGowan JE Jr.
Extra charges and prolongation of stay attributable to nosocomial infections: a prospective interhospital comparison. Am J Med. 1981;70:51-58.
6. Munro CL, Grap MJ. Oral health and care in the intensive care unit: state
of the science. Am J Crit Care. 2004;13:25-33.
7. Munro CL, Grap MJ, Hummel R, Elswick RK, Sessler C. Oral health status: effect on VAP [abstract]. Am J Crit Care. 2002;11:280.
8. Craven DE, Driks MR. Nosocomial pneumonia in the intubated patient.
Semin Respir Infect. 1987;2:20-33.
9. Torres A, el-Ebiary M, Gonzalez J, et al. Gastric and pharyngeal flora in
nosocomial pneumonia acquired during mechanical ventilation. Am Rev
Respir Dis. 1993;148:352-357.
10. Greene R, Thompson S, Jantsch HS, et al. Detection of pooled secretions
above endotracheal-tube cuffs: value of plain radiographs in sheep cadavers
and patients. AJR Am J Roentgenol. 1994;163:1333-1337.
11. Valles J, Artigas A, Rello J, et al. Continuous aspiration of subglottic
secretions in preventing ventilator-associated pneumonia. Ann Intern Med.
1995;122:179-186.
12. Abele-Horn M, Dauber A, Bauernfeind A, et al. Decrease in nosocomial
pneumonia in ventilated patients by selective oropharyngeal decontamination (SOD). Intensive Care Med. 1997;23:187-195.
13. Johanson WG Jr, Seidenfeld JJ, de los Santos R, Coalson JJ, Gomez P.
Prevention of nosocomial pneumonia using topical and parenteral antimicrobial agents. Am Rev Respir Dis. 1988;137:265-272.
14. Scannapieco FA, Stewart EM, Mylotte JM. Colonization of dental plaque
by respiratory pathogens in medical intensive care patients. Crit Care
Med. 1992;20:740-745.
460
15. Kaplan MD, Baum BJ. The functions of saliva. Dysphagia. 1993;8:225-229.
16. Lamkin MS, Oppenheim FG. Structural features of salivary function. Crit
Rev Oral Biol Med. 1993;4:251-259.
17. Rudney JD, Krig MA, Neuvar EK, Soberay AH, Iverson L. Antimicrobial
proteins in human unstimulated whole saliva in relation to each other, and
to measures of health status, dental plaque accumulation and composition.
Arch Oral Biol. 1991;36:497-506.
18. Dawes C. An analysis of factors influencing diffusion from dental plaque into
a moving film of saliva and the implications for caries. J Dent Res. 1989;
68:1483-1488.
19. Torres A, Aznar R, Gatell JM, et al. Incidence, risk, and prognosis factors of
nosocomial pneumonia in mechanically ventilated patients. Am Rev Respir
Dis. 1990;142:523-528.
20. Torres A, Gatell JM, Aznar E, et al. Re-intubation increases the risk of
nosocomial pneumonia in patients needing mechanical ventilation. Am J
Respir Crit Care Med. 1995;152:137-141.
21. Fitch JA, Munro CL, Glass CA, Pellegrini JM. Oral care in the adult intensive care unit. Am J Crit Care. 1999;8:314-318.
22. Pellegrini JM, Fitch JA, Munro CL, Glass CA. Oral hygiene in the intensive care unit: interdisciplinary approach to oral health. J Pract Hyg. JulyAugust 1997;6:15-17.
23. Pugin J, Auckenthaler R, Mili N, Janssens JP, Lew PD, Suter PM. Diagnosis of ventilator-associated pneumonia by bacteriologic analysis of bronchoscopic and nonbronchoscopic “blind” bronchoalveolar lavage fluid. Am
Rev Respir Dis. 1991;143:1121-1129.
24. Fartoukh M, Maitre B, Honore S, Cerf C, Zahar JR, Brun-Buisson C. Diagnosing pneumonia during mechanical ventilation: the Clinical Pulmonary
Infection Score revisited. Am J Respir Crit Care Med. 2003;168:173-179.
25. Singh N, Gayowski T, Wagener MM, Marino IR. Pulmonary infiltrates in
liver transplant recipients in the intensive care unit. Transplantation.
1999;67:1138-1144.
26. Cook DJ, Walter SD, Cook RJ, et al. Incidence of and risk factors for ventilator-associated pneumonia in critically ill patients. Ann Intern Med.
1998;129:433-440.
27. Yende SP, Wunderink RG. Clinical pulmonary infection score [abstract].
Am J Respir Crit Care Med. 1998;114:324S.
28. Papazian L, Thomas P, Garbe L, et al. Bronchoscopic or blind sampling
techniques for the diagnosis of ventilator-associated pneumonia. Am J
Respir Crit Care Med. 1995;152:1982-1991.
29. Langer M, Cigada M, Mandelli M, Mosconi P, Tognoni G. Early onset pneumonia: a multicenter study in intensive care units. Intensive Care Med.
1987;13:342-346.
30. Bauer TT, Ferrer R, Angrill J, Schultze-Werninghaus G, Torres A. Ventilator-associated pneumonia: incidence, risk factors, and microbiology. Semin
Respir Infect. 2000;15:272-279.
31. Fourrier F, Duvivier B, Boutigny H, Rourrel-Delvallez M, Chopin C. Colonization of dental plaque: a source of nosocomial infections in intensive
care unit patients. Crit Care Med. 1998;26:301-308.
32. El-Solh AA, Pietrantoni C, Bhat A, et al. Colonization of dental plaques: a
reservoir of respiratory pathogens for hospital-acquired pneumonia in institutionalized elders. Chest. 2004;126:1575-1582.
AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5
D ownloa de d from a jcc.aacnjournals.org by on August 20, 2009
http://ajcc.aacnjournals.org