Aspiration pneumonia occurs when a large volume of oropharyngeal or gastric contents are aspirated into the lungs, depositing a large bacterial inoculum. This can overwhelm normal lung defenses and cause pneumonia. Risk factors include dysphagia, altered mental status, vomiting, enteral feeding, and oropharyngeal colonization with more virulent bacteria. Aspiration is common but often does not cause pneumonia due to protective mechanisms; however, large volume macroaspiration can lead to aspiration pneumonia.
2. Given this broad use of the term aspiration, classifying the
majority
of bacterial pneumonias as a consequence of aspiration is
strictly
correct based on known pathophysiology of community-
acquired
(CAP) and hospital-acquired pneumonia (HAP) [2–5].
However, when
a clinician uses the term aspiration pneumonia, he or she is
typically
implying a subset of bacterial pneumonia that, although
sharing the
common pathophysiologic mechanism with most other
pneumonias,
represents a unique entity of a macroaspiration event resulting
in
3. It is important to understand that aspiration is a
common event
that may lie within the spectrum of normal
physiology. A large
proportion of healthy people with normal mental
status aspirate
during sleep based on the detection of radiolabeled
oral dyes in the
lungs of healthy volunteers
4. Therefore, one of
the most common consequences of aspiration is
actually to have no
consequence—the inoculum is cleared by the
normal airway and/or
parenchymal host defenses without overt clinical
syndromes.
5. Although occurring in otherwise healthy people,
several important
clinical consequences of aspiration can occur.
6.
7. Chemical Pneumonitis
Chemical pneumonitis is characterized by
macroaspiration of
noxious liquids with immediate hypoxemia, fever,
tachycardia, and
abnormal chest radiograph and lung examination
result. The most
common noxious fluid is sterile gastric contents,
although others such
as bile and other agents instilled into the stomach
may also result in
this syndrome.
8. Animal experiments helped differentiate the pathophysiology
of
chemical pneumonitis from subclinical aspiration based on the
pH
and volume of gastric material needed to stimulate an
immediate and
severe inflammatory reaction. Based on experiments using
human
gastric secretions and rabbit lungs, a pH less than 2.4 was
required to
cause vigorous inflammation. At higher pH, the reaction seen
microscopically was more similar to the changes caused by
the
instillation of water into the lungs [21]. In terms of quantity,
experiments inducing chemical pneumonitis in a dog model
required
2 mL of hydrochloric acid solution per kilogram to induce the
clinical
9. Bland aspiration
Not all noninfectious macroaspirations cause an inflammatory
response in the lung; and therefore, to label these as
pneumonitis
would be inappropriate. Probably the 2 most common
examples are
aspiration of blood as a complication of severe epistaxis or
hematemesis and the aspiration of enteral feedings. Twenty
percent
of patients undergoing esophagogastroduodenoscopy will
have an
infiltrate immediately after the procedure in the dependent lung
[24,25]. Most resolve without antibiotic changes. Most
episodes of
aspiration with enteral nutrition are also uncomplicated
10. Although bland aspiration may not initially be infectious, blood
and enteral feedings represent excellent culture media for
growth of
either resident bacteria or the small aliquot of bacteria
included in the
inoculum. Generally, mucociliary clearance and the resident
alveolar
macrophages can clear the inoculum within hours. The major
issue is
confusion with an infectious aspiration pneumonia, particularly
when
the large-volume aspiration is not observed. Prolonged
antibiotic
treatment is unlikely to prevent this secondary pneumonia but
may
select for more multidrug-resistant (MDR) pathogens
11. CAP & HAP
Microaspiration has long been known to be the dominant
pathophysiologic mechanism behind CAP. Supporting evidence
includes the finding that most common CAP-causing microorganisms
colonize the oropharynx or nasopharynx in nonhospitalized patients
[2,27,28]. Similarly, the pathophysiology underlying HAP, including
ventilator-associated pneumonia (VAP), has proved to be microaspiration
of oropharyngeal, upper gastrointestinal, or subglottic
contents [3,5,29–32]. The distinct microbiology of HAP stems from
microaspiration occurring after hospitalized patients become colonized
with the virulent organisms found in intensive care unit and
hospital environments [4,33–36].
Given the above evidence of aspiration as a common event,
development of a parenchymal lung infection depends largely on host
defense factors [12,37] and the virulence of the aspirated pathogen.
This interaction helps explain the phenomenon of subclinical
aspiration without subsequent pneumonia described mostly in
young healthy volunteers and surgical candidates
12. Aspiration Pneumonia
Current use of this term most commonly refers to an acute
lung
infection developing after a large-volume aspiration of
oropharyngeal
or upper gastrointestinal contents with a high enough pH to
avoid
chemical pneumonitis (likely pH much greater than 2.5). This
type of
aspiration deposits a large bacterial load of pathogens from
the oral
cavity or upper gastrointestinal tract into the lungs. The
possibility of
infection with these normally nonvirulent, predominantly
anaerobic
organisms is partly because of the large inoculum
[2,17,21,39–41].
Confusion surrounding this terminology and the exact
definition
13. Macroaspiration is the unique pathophysiologic
component of
what most clinicians call aspiration pneumonia. The
challenge in
specifically diagnosing aspiration pneumonia is that, for
many
patients in the community who are at risk for
macroaspiration, the
events in the days leading up to presentation with fever,
cough, and
chest radiograph infiltrate are unclear. A common risk for
macroaspiration
is decreased mental status, but this can be the result of
CAP
rather than the cause [43]. Because of this reality,
substantial
diagnostic overlap exists between aspiration, HAP, and
14. Aspiration pneumonia represents 5% to 15% of
pneumonias in the
hospitalized population. The ICD-9 code–based
reviews suggest an
increasing incidence, making it the second most
common diagnosis in
Medicare patients who are hospitalized [2,44].
However, higher
reimbursement rates for this ICD-9 code than for
CAP ICD-9 codes may
falsely increase the frequency in this population.
15. RFs for Aspiration Pneumonia
Specific predisposing factors for aspiration pneumonia focus
on
the risk for high frequency and/or large volume of aspiration.
Some
risks may be more pertinent for the macroaspiration
characteristic of
aspiration pneumonitis or anaerobic pleuropneumonia than for
microaspiration. Additionally, factors that influence the resident
bacterial flora leading to colonization by more virulent
pathogens,
which are more likely to overwhelm the normal protective
mechanisms,
also play a role in development of clinical disease
16. RFs for Aspiration Pneumonia
Dysphagia/swallowing dysfunction
Dysphagia, typically from neurologic disease
(dementia, Parkinson
disease, multiple sclerosis, poststroke), is
considered the most
important risk factor for aspiration pneumonia, given
the abovedescribed
pathogenesis.
17. RFs for Aspiration Pneumonia
Dysphagia/swallowing dysfunction
It is important to remember that dysphagia itself is not
definitive
evidence of aspiration. Many high-risk patients will not
complain of
dysphagia but still aspirate based on advanced testing [51].
The
poststroke population certainly has a higher prevalence of
pneumonia
with or without symptomatic dysphagia [52,53]. A lag time of
more
than 5 seconds between noxious stimuli and cough, as well as
an
increasing stimuli needed to produce a cough, has been linked
to
pneumonia in poststroke patients regardless of dysphagia
18. RFs for Aspiration Pneumonia
Dysphagia/swallowing dysfunction
The swallowing mechanism can also be affected by
chest anatomy.
Swallowing dysfunction is very common in chronic
obstructive
pulmonary disease (COPD) patients with
hyperinflation
19. RFs for Aspiration Pneumonia
Dysphagia/swallowing dysfunction
Certain medications interfere with the swallow reflex
and may
potentially lead to aspiration [58]. Although sedatives
may suppress
the patient’s mental status sufficiently to lead to
aspiration,
antipsychotic medications may actually affect the
swallowing mechanism
by inhibiting dopamine and therefore lead to
aspiration.
Accordingly, these drugs have been linked to
pneumonia in a fairly
large retrospective study
20. RFs for Aspiration Pneumonia
Altered Mental Status
The association between acute altered mental status
(AMS) and
aspiration pneumonia has not been studied extensively
despite the
obvious connection
Most available case series focus on the association of
acute AMS with chemical pneumonitis in the setting of
sedation,
poisoning, and trauma In these populations, vomiting and
large-volume reflux of gastric contents may also increase
the risk of
aspiration pneumonia.
21. RFs for Aspiration Pneumonia
Altered Mental Status
Two specific types of AMS—acute alcohol abuse and
seizures—are
most likely to lead to the anaerobic pleuropneumonia
syndrome.
Probably the highest risk of aspiration pneumonia
occurs in the severe
alcohol abuse population. Acute alcohol ingestion
has multifactorial
risks for aspiration pneumonia including AMS,
increased risk of
vomiting, and direct effects of alcohol on normal
neutrophil function.
22. RFs for Aspiration Pneumonia
Esophogeal motility disorders/vomiting
Esophogeal motility disorders independent of GERD are also
associated with aspiration and an increased risk of
pneumonia.
Many are a component of an underlying systemic disease,
such as
scleroderma or polymyositis, which may also compromise the
host
immune response itself or secondary to immunosuppressive
treatment.
Primary esophageal disorders, such as achalasia and
esophageal
strictures, increase the risk of aspiration of not only liquids but
also
solids. The latter are a unique form of aspiration risk in which
bronchial impaction and postobstructive pneumonia result
from the
23. RFs for Aspiration Pneumonia
Esophogeal motility disorders/vomiting
Given the frequency of vomiting, the incidence of
aspiration
pneumonia/pneumonitis is actually very low.
Protective laryngeal
reflexes will prevent macroaspiration in the
overwhelming majority
of circumstances. Macroaspiration with vomiting
almost always
requires concomitant abnormal mental status, such
as anesthesia
induction, acute alcohol intoxication, or
narcotics/sedatives.
24. RFs for Aspiration Pneumonia
Esophogeal motility disorders/vomiting
Another unique syndrome is vomiting associated with
small bowel
obstruction. In this situation, the stomach is no longer
sterile but
instead is filled with fluid that has significant overgrowth
of bowel
flora. Narcotics and antiemetics may compromise mental
status at the
time of vomiting. The result is a fulminant aspiration
pneumonia due
to gram-negative bowel pathogens, rather than the
predominant
gram-positive/anaerobic oral flora.
25. RFs for Aspiration Pneumonia
Enteral feeding
The risk for aspiration pneumonia with enteral tube
feeding has
been extensively studied, especially in the more
critically ill. Smalland
large-bore nasogastric tubes, postpyloric tube feeds,
gastric tube
feeds, and jejunal tube feeds have all been
associated with aspiration
pneumonia in patients with and without endotracheal
and tracheostomy
tubes.
26. RFs for Aspiration Pneumonia
Enteral feeding
Exact risk is difficult to characterize given the wide
variety of incidences reported, small sample sizes,
and lack of
standard definitions regarding aspiration and
aspiration pneumonia
[65–75]. Regardless of the deficiencies in
epidemiologic data,
aspiration pneumonia is common enough in this
population that it
should be a consideration for all patients on tube
feeds.
27. RFs for Aspiration Pneumonia
Enteral feeding
Certain
patients appear to be at greater risk. Intuitively, GERD and
decreased
gastric motility are implicated when tube feeds are aspirated
Decreased gastric motility, typically defined by high gastric
residual volume, has also been suggested as a risk factor for
aspiration
in tube-fed patients [65,67]. However, the criteria for high
gastric
residual volume vary widely between studies from 50 to
greater than
500 mL at every 4-hour checks. A potentially independent risk
factor
is that patients with high gastric residuals may also be at
increased
risk of vomiting
28. RFs for Aspiration Pneumonia
Oropharyngeal colonization
Microbiologic factors also influence the risk of aspiration
pneumonia.
Pathophysiologically, risk of pneumonia relates to the
body’s
ability to combat the bacteria that routinely reach the
lower
respiratory tract. Unusual or more virulent microbes may
be more
difficult to eradicate by the normal host defenses. By far,
the most
important influence on alterations in normal
oropharyngeal flora is
use of systemic antibiotics.
29. RFs for Aspiration Pneumonia
Oropharyngeal colonization
An independent association of poor oral hygiene with
aspiration
pneumonia is also supported by the literature [56,77]. The
microbial
density is increased in patients with gingival disease even if
the
spectrum has not shifted, increasing the likelihood of
pneumonia
developing in association with an episode of aspiration due to
the
greater inoculum. This suggests that edentulous patients are
at lower
risk for aspiration pneumonia. In edentulous patients, the
tongue is
more important as a focal point for colonization. Abe et al [78]
associated tongue-coating scores in an edentulous elderly
30. RFs for Aspiration Pneumonia
Oropharyngeal colonization
Many of the studies of oral hygiene have also
demonstrated greater
colonization by more virulent organisms in patients
with poor oral
hygiene. This is especially true for the colonization of
gram negatives
and respiratory pathogens in the intensive care unit [
31. RFs for Aspiration Pneumonia
Other Risks
Other risks
General risk factors like male sex and smoking may
increase risk
for aspiration pneumonia based on case-controlled and
cohort studies
[48]. Diabetes mellitus has been repeatedly associated
with pneumonia
in patients who have had an acute stroke [48].
Much has been discussed regarding the increased risk of
pneumonia as a whole in patients being treated with
proton pump
inhibitors and/or histamine receptor–2 antagonists
[80,81].
32. RFs for Aspiration Pneumonia
Other Risks
Although
these medications may not increase the risk of aspiration, they
change
the gastrointestinal environment such that natural host
defenses,
which include gastric acid secretion, cannot reduce bacterial
burden. If
a subsequent aspiration event occurs, patients appear more
likely to
deliver an inoculum of bacteria high enough to cause clinical
infection.
Conversely, the frequent use of proton pump inhibitors or
histamine
receptor–2 antagonist, particularly in the hospitalized
population,
may be associated with a lower incidence of aspiration
pneumonitis
33. Diagnosis
In clinical practice, aspiration pneumonia is
most often coded as the diagnosis when a new chest
radiograph
infiltrate in a dependent pulmonary segment is found
in patients with
risk factors for aspiration. In a bed-bound patient, the
dependent
pulmonary segments are the posterior segments of
the upper lobes
and the superior segments of the lower lobes. In
ambulatory patients,
lower lobes are classically involved, especially the
right
34. Diagnosis
Clinical features can help distinguish aspiration pneumonia
from
chemical pneumonitis and other lung infections. As opposed to
chemical pneumonitis, the aspiration event in aspiration
pneumonia
is rarely witnessed [17]. The large volume of stomach contents
required to cause chemical pneumonitis usually makes it a
more
obvious event. Furthermore, the clinical course of chemical
pneumonitis
is hyperacute hypoxemia, occurring almost immediately (within
hours) and resulting in either devastating lung injury or
resolution
within 48 hours. These patients are likely to also have
bronchospasm,
frothy sputum, and chest radiographs with bilateral patchy
infiltrates
including nondependent areas
35. Diagnosis
Because of this difficulty, efforts have been made to
use biomarkers
to distinguish aspiration pneumonia from other
aspiration syndromes.
El-Solh et al [85] attempted to use procalcitonin to
distinguish aspiration pneumonitis from aspiration
pneumonia in
the intensive care unit setting, given data to suggest
that procalcitonin
is a helpful marker for bacterial causes of sepsis
36. Diagnosis
Unfortunately, no difference between procalcitonin
levels was demonstrated in
culture-negative and culture-positive patients.
37. Diagnosis
Biomarkers more specific to aspiration have also been
studied.
Pepsinogen in tracheal secretions or BAL was very suggestive
of
aspiration as part of the pathogenesis of posttransplant BO
and VAP.
Bronchoalveolar lavage amylase levels have been
demonstrated to
correlate with clinical risk factors for aspiration, as well as with
positive cultures [87–89]. This relationship may even be true in
patients with VAP [90]. Bronchoalveolar lavage amylase can
also
function as an end point for studies of interventions to
decrease risk of
aspiration in ventilated patients
38. Microbiology
The unique pathophysiology of aspiration
pneumoniamay lend itself
to unique pathogens. However, the microbiology,
and therefore the
treatment, has seen significant changes over the last
40 to 50 years.
39. The original teaching was that anaerobic bacteria
were by far the
most common pathogens in aspiration pneumonia
based on well-done
microbiology studies undertaken in patientswith
aspiration pneumonia
acquired in and out of the hospital fromthe 1960s to
1980s.*
40. These anaerobic infections
commonly included greater than one pathogen, with
Bacteroides
species, Prevotella, Fusbacterium species, and
peptostreptococci predominating
(Table 2). Most of these patients had the anaerobic
pleuropneumonia syndrome described above.
41.
42. As homogenous as these initial results appeared, evidence
accumulated
that aspiration pneumonia occurring after hospitalization had a
microbiologic
spectrum that included more Staphylococcus aureus, aerobes,
and gram-negative bacilli [17,84,92,94]. The pathogens that
dominate aspiration
pneumonia microbiology after a macroaspiration event after
hospitalization are similar to those of many nosocomial
infections.
Although very limited, data fromreliable cultures in
nonintubated patients
do suggest a higher frequency of anaerobes than in intubated
patients; but
the frequency is substantially lower than that of the prior
43. Recent studies reveal much different results even for
patients
presenting from the community. El-Solh et al [97]
reported a series of
patients with suspected aspiration pneumonia who
underwent
bronchial sampling after intubation. Of the 54
patients with a
bacterial diagnosis, 20% grew only anaerobes, with
an additional
11% that included anaerobes as part of mixed flora.
44. In contrast,
common causative organisms in this study were
Escherichia coli,
S aureus, and Klebsiella pneumoniae. Tokuyasu et al [98]
described this
trend further in a series of elderly Japanese patients with
clinically
diagnosed aspiration pneumonia. Of 111 organisms
isolated in 62
individuals, only 22 (20%) were anaerobes. Anaerobes
were heavily
outweighed by gram-negative bacilli (almost all enteric
gramnegatives),
found in 51.6% of patients
45. Even the etiology in patients with lung abscess has changed.
Takayanagi et al [99] reported bacterial etiologies in 122
patients
diagnosed with community-acquired lung abscess, likely a
result of
untreated aspiration. In this population, 74% grew aerobes
only, 12%
grew anaerobes only, and 14% grew mixed flora. Of the 107
aerobic
cases, 79% were Streptococcus species. In a very similar
study, Wang et
al [100] reported that only 40 (44%) of 90 community-acquired
lung
abscesses grew any anaerobes, with only 13% purely
anaerobic. Of the
remaining cases, 33% were caused by K pneumoniae (almost
all being
pure K pneumoniae isolates).
46. The latter finding suggests that
aspiration may not even play a role in some cases of
lung abscess,
but rather more virulent CAP pathogens. The
combination of lung
abscess and empyema has also been reported with
communityacquired
methicillin-resistant S aureus (MRSA) pneumonia
47. These 2 distinct bodies of literature, taken
chronologically, reveal a
fading importance of anaerobic bacteria in aspiration
pneumonia and even community-acquired lung abscess.
A second implication of this
etiologic shift is that the principles of typical nosocomial
microbiology
apply to patients with aspiration pneumonia if
macroaspiration
occurs after hospitalization. This etiologic overlap
between aspiration
pneumonia and HAP has been progressively evident
since the 1970s
48. Treatment
As one would expect, empirical treatment of aspiration
pneumonia
has evolved, given the above changes in the microbiology of
the
infection [102]. Intravenous penicillin was the drug of choice in
the
past, as anaerobes constituted the vast majority of infections
with few
penicillinase-producing bacterial strains [103,104]. A
randomized
controlled trial (RCT) of 39 patients with lung abscesses
compared
penicillin with clindamycin in the early 1980s [105]. Although a
small
group of patients, the treatment failure rate and cure rate were
much
better for clindamycin, with all 13 followed patients being cured
vs 8
49. The failure of penicillin to cure anaerobic
infections was better characterized several years
later in a Spanish
RCT of confirmed anaerobic lung infections [106]. In
this cohort of 37
patients, 47 anaerobes were isolated. Ten of these
47, all Bacteroides
species, were penicillin resistant, whereas none
were clindamycin
resistant. None of the 5 patients with penicillin-
resistant bacteria
randomized to penicillin responded to therapy.
50. Metronidazole has also been studied in anaerobic lungs
infections.
Sanders et al [107] described a poor cure rate in 13
patients with
pleuropulmonary (11 of 13 being lung abscesses)
infections with
confirmed anaerobic bacteria. Similarly, Perlino [108]
reported higher
cure rates with clindamycin when compared to
metronidazole in
cases of lung abscess and pneumonia with confirmed
anaerobic flora
in a small RCT of 13 patients.
51. It is important to understand that these studies included
mainly
classic anaerobic pleuropneumonia syndrome with
anaerobes confirmed
on culture and that most were completed decades ago. In
the
currently uncommon patient with aspiration resulting in
classic
anaerobic pleuropneumonia, prior results and the likely
greater
incidence of penicillin resistance suggest that
clindamycin may be
the optimal agent
52. Recent studies have focused on pneumonia in patients with
risk
factors for aspiration. Kadowaki et al [109] randomly assigned
100
elderly Japanese patients with suspected aspiration
pneumonia to
clindamycin, a carbapenem (penipenem/betamiprom), low-
dose
ampicillin/sulbactam (1.5 g twice daily), or high-dose
ampicillin/
sulbactam (3 g twice daily). The investigators found little
variance in
efficacy (N75% cure rate in all groups) and adverse events.
Interestingly,
no anaerobes were actually cultured. Of note, clindamycin was
the
53. Another study of elderly Japanese
with aspiration pneumonia [98] demonstrated a clinical
efficacy rate of
61.3% with another carbapenem, meropenem. This lower
efficacy than
that found by Kadowaki et al [109] may be due to greater
severity of
illness in the study patients. Once again, nosocomial
pathogens rather
than anaerobes were the most common documented
etiologies; and 33
of these 62 patients had MRSA growing in their
postantibiotic sputum
culture.
54. A recent randomized German study compared high-dose
ampicillin/sulbactam (3 g thrice times daily) to the standard
CAP
antibiotic moxifloxacin for the treatment of aspiration
pneumonia and
lung abscess in 96 elderly patients [110]. Clinical response
rates were
identical at 66.7%, and adverse reaction rates were very
similar.
Microbiology was consistent with the more recent data
described
above, with less than 10% of bacteria cultured being
anaerobes. Of note,
higher (although not statistically significant) mortality was seen
in the
ampicillin/sulbactamgroup, with 14 patients dying compared to
6 in the
moxifloxacin group.
55. These recent data from Japan and Germany have
demonstrated
effective treatment strategies for aspiration
pneumonia in the face of new microbiology patterns.
Based on this limited evidence,
clindamycin, a carbapenem, ampicillin/sulbactam,
and moxifloxacin
all appear to be reasonable first-line therapies in
modern-day
community-acquired aspiration pneumonia
56. For patients with hospital-acquired macroaspiration
pneumonias,
use of broad-spectrum combination therapy is
recommended if MDR
risk factors are present. Probably the single most
important risk factor
for MDR pathogens is prior antibiotic treatment. If none,
the
antibiotics listed for community-acquired aspiration
pneumonia are
adequate. The longer the prior course and the broader
the spectrum of
agent, the greater the likelihood of MDR pathogens.
57. In nonventilated
patients, anaerobes may still play a role; and
cefepime should be
avoided. For ventilated patients, the high oxygen
tension is sufficient
to kill anaerobes; and any β-lactam should be
appropriate, although
changing β-lactam class may be prudent.
58. Prevention
Dietary Changes
Dietary interventions have been studied in patients with dysphagia.
In a small study involving patients with dysphagia secondary to
neurodegenerative disease (pseudobulbar dysphagia) [111], more
aspiration pneumonia occurred in those on a pureed diet compared
to
a mechanical soft diet with thickened liquids. However, the utility of
dietary intervention has been questioned. Depippo et al [112]
randomized 115 poststroke patients to 3 groups according to speech
therapist intervention: Group A was given advice based on swallow
testing, but the ultimate dietwas determined by the patient and
family;
Group B was prescribed a specific diet based on swallow testing;
and
Group C was prescribed a specific diet and directly observed for
compliance daily. No statistically significant differences between the
groups were found in any end point.
59. Prevention
Drugs to Protect the Airway
A number of small studies have reviewed
pharmacologic intervention
to protect the airway via the cough reflex. The most
interesting drugs studied are angiotensin-converting
enzyme inhibitors
(ACEIs) because of their role in degrading substance
P and
bradykinin, stimulants of the cough reflex. A
reduction in aspiration
pneumonia in patients on an ACEI has been
suggested in one casecontrol
study [113] in elderly Japanese patients
60. Prevention
Drugs to Protect the Airway
Further, investigators
have categorized an increased risk for pneumonia in
patients with
certain ACE gene polymorphisms that are
associated with higher ACE
levels: homozygous deletion of an alu repeat within
intron 16 (ACE
DD). The risk of pneumonia was markedly reduced
in a case-control
study of patients without this genotype who were
taking an ACEI,
whereas it was unaffected in patients with the
genotype
61. Prevention
Enteric Feeding Tubes
Because enteric tube feeding presents a risk for
aspiration, there has
been considerable effort to compare types of tube
feeds tominimize this
risk. The most important comparisons are between
gastric and
postpyloric feedings. Given the gastric dysmotility
caused by critical
illness, gastroparesis, and commonmedications,
postpyloric feeds have
been commonly postulated to be superior
62. Prevention
Enteric Feeding Tubes
Two small prospective
trials have found no difference [115,116] in
pneumonia rates. To the
contrary, a very small randomized trial, with almost
no cases of
aspiration pneumonia, and another prospective trial
found advantages
to jejunal feeds [117,118]. Comparisons have also
been made between
nasogastric tube and percutaneous endoscopic
gastrostomy tube feeds
in a variety of clinical settings.
63. Prevention
Enteric Feeding Tubes
Several randomized controlled trials have
failed in demonstrating a difference in pneumonia
complication rates
between the 2 feeding strategies. Percutaneous
endoscopic gastrostomy
tubes are more likely to achieve goal feeds but come
at a much higher
cost
64. Prevention
Enteric Feeding Residual Volumes
Many institutions monitor residual volumes from tube
feeds to
know when aspiration risk is increased. Residual
volumes of 500 mL are considered high enough to hold
tube feeds [65]. However, the
inaccuracy of this method has been well documented
[122].
Furthermore, results from a recent randomized clinical
trial suggest
that using strict residual volumes (250 mL) to understand
when to
hold nasogastric tube feeds does not affect the incidence
of VAP
65. Prevention
Oral Care
Oral care has been shown to assist in preventing
aspiration
pneumonia as expected given the evidenced
discussed above. Data are
again limited, but encouraging quality oral care offers
potential
benefit with almost no morbidity
66. Prevention
Prophylactic Antibiotics
For patients at risk of aspiration around the time of
endotracheal
intubation, several studies have shown that a short
course (≤24
hours) of “prophylactic” β-lactam antibiotics may
decrease the risk of
subsequent VAP [125,126]. An extremely elevated
BAL amylase may
better select patients for this intervention.
67. Prevention
Head Elevation
One very important preventative measure surrounds
preventing
aspiration in the hospitalized, critically ill patient.
Increased aspiration
in the supine position was evident after a Spanish study
that detected
enterically administered dye aspirated into the lungs of
mechanically
ventilated patients. Aspiration rates not only were higher
in patients
who were supine but were dependent on how much time
was spent
in the supine position
68. Prevention
Head Elevation
The same investigators then confirmed
the importance of this phenomenon by demonstrating
drastically
reduced rates of HAP in mechanically ventilated patients
in the
semirecumbent position compared to supine [128]. A
subsequent
study did not show a benefit of semirecumbant position
when
compared to elevation of as little as 10° from supine
[129]. However,
the risk benefit ratio of elevation of the head of the bed in
ventilated
patients is so favorable that it has become standard
practice
Bartlett and
Gorbach [17] and Bartlett et al [92] reported on 2 cohorts of patients:
one with aspiration pneumonia and a second with aspiration-induced
pulmonary infections including pleural. In the initial study, 50 (93%) of
54 patients had anaerobes (25 cultures grewonly anaerobes; 25were a
part of mixed flora). In the follow-up study, 61 (87%) of 70 patientswith
aspiration pneumonia had anaerobes in culture. Subsequent studies
[93–96] seemed to confirm these results.