Aspiration pneumonia in adults

Author: Michael Klompas, MD, MPH

Section Editor: Daniel J Sexton, MD
Deputy Editors: Jennifer Mitty, MD, MPH, Sheila Bond, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2025. | This topic last updated: Oct 04, 2024.

INTRODUCTION
Aspiration pneumonia refers to adverse pulmonary consequences due to entry of
gastric or oropharyngeal fluids, which may contain bacteria and/or be of low pH, or
exogenous substances (eg, ingested food particles or liquids, mineral oil, salt or fresh
water) into the lower airways [1].
The predisposing conditions, clinical syndromes, diagnosis, and treatment of
aspiration pneumonia will be reviewed here. Community-acquired pneumonia,
hospital-acquired pneumonia, empyema, and lung abscess are discussed separately.
● (See "Overview of community-acquired pneumonia in adults".)
● (See "Clinical presentation and diagnostic evaluation of ventilator-associated
pneumonia".)
● (See "Treatment of hospital-acquired and ventilator-associated pneumonia in
adults".)
● (See "Lung abscess in adults".)

DEFINITIONS
The term aspiration pneumonia should be reserved specifically for pneumonitis
resulting from aspiration of oropharyngeal or gastric contents ( table 1). This is
typically due to impairment of the clearance defenses (eg, depressed sensorium,
glottic closure, or cough reflex). The character of the inoculum, underlying pulmonary
conditions, and presentation assist in distinguishing the three most common clinical
syndromes within the category of aspiration pneumonia, namely chemical
pneumonitis, bacterial infection, and airway obstruction [2]. Although there may
occasionally be overlap and it is often difficult to classify individual cases with
certainty, this classification scheme is essential to understanding and managing
aspiration pneumonia.
● Chemical pneumonitis refers to the aspiration of substances (eg, acidic gastric
fluid) that cause an inflammatory reaction in the lower airways, independent of
bacterial infection.
● Bacterial aspiration pneumonia refers to an active infection caused by inoculation
of large amounts of bacteria into the lungs via orogastric contents. These
bacteria may be aerobic, anaerobic or a mixture. Risk factors for aspiration
pneumonia include neurologic disorders, reduced consciousness, esophageal
disorders, vomiting, and witnessed aspiration [3].
The distinction between bacterial pneumonia and bacterial aspiration pneumonia
is imprecise because most pneumonias are presumed to be caused by aspiration
[4,5]. Bacterial aspiration pneumonia is classically applied to pneumonia that
develops following a witnessed or presumed large volume inoculation of
orogastric contents into the lungs, whereas bacterial pneumonia is presumed to
be secondary to subclinical microaspirations of oral flora. These events likely
occur on a continuum, however, and the distinction between them is somewhat
arbitrary.
● Mechanical obstruction – Aspiration of fluid or particulate matter that obstructs
the airway or triggers reflex airway closure but without an associated
parenchymal inflammatory reaction.
An alternative classification is "aspiration pneumonitis" in reference to lung injury due
to gastric acid and "aspiration pneumonia" in reference to pneumonia due to bacterial
infection [6].

PREDISPOSING CONDITIONS
Aspiration of small amounts of oropharyngeal secretions is common even in healthy
individuals and usually resolves without detectable sequelae [7]. Sensitive tests show
that at least one-half of healthy adults aspirate during sleep [4,8]. Thus, most
episodes of aspiration are subclinical and rapidly resolve without clinical
manifestations. The small fraction of aspiration events that do proceed to clinically
manifest disease appears to depend upon the volume and contents of the inoculum
as well as failures of host defense mechanisms.
Conditions that predispose to aspiration include processes that reduce consciousness,
interfere with normal swallowing, impair airway clearance (ciliary function or cough),
or lead to frequent or large-volume aspiration ( table 2) [1,9]. Conditions that lead to
frequent or large-volume aspiration also increase the probability of aspiration
pneumonitis ( table 2). Examples include the following:
● Reduced consciousness (eg, due to sedative or antipsychotic medications, alcohol
or drug use, anesthesia, generalized seizures) can compromise the cough reflex
and glottic closure [1,9,10].
● Dysphagia from neurologic deficits. (See "Swallowing disorders and aspiration in
palliative care: Definition, pathophysiology, etiology, and consequences".)
● Disorders of the upper gastrointestinal tract including esophageal disease,
surgery involving the upper airways or esophagus, and gastric reflux. (See
"Approach to the evaluation of dysphagia in adults".)
● Mechanical disruption of the glottic closure or lower esophageal sphincter due to
tracheostomy, endotracheal intubation, head and neck cancer, bronchoscopy,
upper endoscopy, and nasogastric feeding.
● Pharyngeal anesthesia and miscellaneous conditions such as protracted
vomiting, large-volume tube feedings, feeding gastrostomy, the recumbent
position, and near-drowning.
● Poor dental hygiene is also associated with increased risk of aspiration
pneumonia, presumably because aspiration in this setting is associated with
higher inoculums of oral flora and potentially a shift to more pathogenic bacteria
[6,11-17]. Poor dental hygiene may also be a marker for other chronic conditions
that predispose to aspiration.
 ● Increasing age is an important risk factor for aspiration pneumonia, largely due
to diseases related to aging (eg, stroke, degenerative neurologic disease, altered
mental status due to medications, frailty), with patients in long-term care facilities
and those with comorbidities being particularly vulnerable [18-20].
● Cardiac arrest has been associated with a particularly high incidence of
pneumonia, presumably due to loss of consciousness as well as aspiration of
oropharyngeal and gastric contents in the context of cardiopulmonary
resuscitation, bag-valve mask ventilation, and emergent intubation [21,22].
While some observational studies have demonstrated an association between use of
acid-suppressive medications and pneumonia (community-acquired pneumonia,
ventilator-associated pneumonia, and hospital-acquired pneumonia), large clinical
trials have not found any difference in ventilator-associated pneumonia rates in
patients randomly assigned to proton pump inhibitor therapy for stress ulcer
prophylaxis [23-25]. (See "Epidemiology, pathogenesis, and microbiology of
community-acquired pneumonia in adults", section on 'Predisposing host conditions'
and "Proton pump inhibitors: Overview of use and adverse effects in the treatment of
acid related disorders", section on 'Pneumonia' and "Stress ulcers in the intensive care
unit: Diagnosis, management, and prevention", section on 'Potential harms'.)
In a prospective population-based study of 1946 patients with pneumonia admitted to
the hospital from continuing care facilities (CCFs) or the community [26], the most
common risk factor for community-acquired aspiration pneumonia was impaired
consciousness due to alcohol, drugs, or hepatic failure, whereas the most common
risk factor for CCF-acquired aspiration pneumonia was neurologic disease that
resulted in dysphagia (present in 72 percent of CCF-acquired aspiration pneumonias).
In another report that included 134 older adult patients (mean age 84 years)
hospitalized with pneumonia, 55 percent had oropharyngeal dysphagia based on a
water swallow test [27].

CHEMICAL PNEUMONITIS
The prototype and best studied clinical example of chemical pneumonitis is that
associated with the aspiration of gastric acid first described by Mendelson in 1946 and
sometimes referred to as Mendelson syndrome [28,29]. Chemical aspiration
pneumonitis also occurs perioperatively, most often during intubation or extubation
for anesthesia or during procedures like laryngoscopy. Pneumonitis due to
hydrocarbon inhalation is described separately. (See "Postoperative airway and
pulmonary complications in adults: Management following initial stabilization",
section on 'Aspiration (chemical) pneumonitis' and "Acute hydrocarbon exposure:
Clinical toxicity, evaluation, and diagnosis".)
Mendelson’s original series included 61 obstetrical patients who aspirated gastric
contents during ether anesthesia [28]. Respiratory distress and cyanosis rapidly
followed, usually within two hours of a witnessed aspiration [29]. Chest radiographs
showed opacities that were usually located in one or both lower lobes. Despite the
initial severity of the illness, all 61 patients had a rapid clinical recovery within 24 to 36
hours, with radiographic resolution within four to seven days without the use of
antimicrobial therapy.
Subsequent studies have shown that this form of aspiration pneumonia occasionally
follows a fulminant course, however, that may result in acute respiratory distress
syndrome (ARDS) [30]. In patients with aspiration pneumonia resulting in ARDS, blood
gas studies usually show that the partial pressure of oxygen (PaO2) is reduced,
accompanied by a normal or low partial pressure of carbon dioxide (PaCO2) with
respiratory alkalosis. Factors that contribute to hypoxemia include noncardiogenic
pulmonary edema, reduced surfactant activity, reflex airway closure, alveolar
hemorrhage, and hyaline membrane formation. Pulmonary function tests show
decreased compliance, abnormal ventilation-perfusion, and reduced diffusing
capacity. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and
complications in adults".)
The difference in the clinical course of chemical pneumonitis reported by Mendelson
compared with some patients included in more recent studies may be explained by
differences in the types of patients included in different series. Mendelson described
healthy, young obstetrical patients, whereas the subjects of subsequent reports were
often older, debilitated, or burdened with comorbid conditions [28,30]. Reporting bias
may have also favored publication of more seriously ill patients, as a contrast to
Mendelson’s original report.
Pathophysiology — The pathophysiology of acid pneumonitis has been studied
extensively in experimental animals using intratracheal installation of acid [31-33].
These animal models demonstrated that an inoculum with a pH of ≤2.5 and relatively
large volume (usually 1 to 4 mL/kg) was needed to cause chemical pneumonitis. This
would translate to an inoculum of at least 70 mL of gastric acid in adult humans. It is
probable that smaller volumes produce a more subtle process that either escapes
clinical detection or causes a less fulminant form of pneumonitis. The clinical
observation that some patients with esophageal or gastric reflux experience frequent
bouts of recurrent pneumonitis, sometimes accompanied by pulmonary fibrosis,
supports this concept [34,35].
The pathologic changes in the preceding animal models of acid pneumonitis evolve
rapidly. Within three minutes, there is atelectasis, peribronchial hemorrhage,
pulmonary edema, and degeneration of bronchial epithelial cells. By four hours, the
alveolar spaces are filled with polymorphonuclear leukocytes and fibrin. Hyaline
membranes are seen within 48 hours. The lung at this time is also grossly edematous
and hemorrhagic with alveolar consolidation.
All of the findings described above have also been noted on autopsy of patients with
fatal aspiration pneumonia. The presumed mechanism is the release of
proinflammatory cytokines, especially tumor necrosis factor (TNF)-alpha and
interleukin (IL)-8 [36-38].
Bile may also elicit an inflammatory response in the lungs and has been found
frequently in endotracheal tubes of patients on ventilators [39].
Clinical features — The following clinical features should raise the possibility of
chemical pneumonitis [1,40,41]:
● Abrupt onset of symptoms, such as dyspnea, cough, hypoxemia, and tachycardia
in a patient with risk factors for aspiration.
● Fever, which may be low-grade.
● Diffuse crackles or wheezes on lung auscultation.
● Opacities on chest imaging involving dependent pulmonary segments ( image 1
and image 2). The dependent lobes in the upright position are the lower lobes.
 However, aspiration that occurs while patients are in the recumbent position may
result in infection in the superior segments of the lower lobes and the posterior
segments of the upper lobes. A minority of patients develop a radiographic
pattern of acute respiratory distress syndrome with diffuse opacities.
Diagnosis — The diagnosis of chemical pneumonitis is usually presumptive based
upon the clinical features and course noted above. After a suspected aspiration event,
chest radiograph abnormalities typically appear within two hours. Bronchoscopy,
although usually not necessary, demonstrates erythema of the bronchi, indicating
acid injury.
Treatment — Patients with an observed aspiration should have immediate
oropharyngeal suctioning with the head turned to the side to prevent further
aspiration, and those with an endotracheal tube in place should have immediate
tracheal suctioning to clear fluids and particulate matter that may cause obstruction.
The chemical injury that occurs with a gastric acid aspiration event occurs instantly in
a manner that has been compared with a "flash burn," which is followed by rapid
release of inflammatory mediators and neutrophil recruitment [42]. Bronchoalveolar
lavage, which may be used to clear particulate matter, will not protect the lungs from
the chemical injury that is already in progress.
● Supportive care – The major therapeutic approach is to support oxygenation and
provide mechanical ventilation for patients with respiratory failure. Supportive
care for patients with acute respiratory distress syndrome (ARDS) is discussed
separately. (See "Acute respiratory distress syndrome: Ventilator management
strategies for adults" and "Acute respiratory distress syndrome: Fluid
management, pharmacotherapy, and supportive care in adults".)
● Systemic glucocorticoids – The routine use of glucocorticoids in the treatment
of chemical aspiration pneumonitis is discouraged, as observational studies in
humans have not demonstrated clear benefit [1,43]. The administration of
glucocorticoids for ARDS is discussed separately. (See "Acute respiratory distress
syndrome: Fluid management, pharmacotherapy, and supportive care in adults".)
● Empiric antibiotics – Clinical studies suggest that 13 to 26 percent of patients
with observed aspiration events acquire pulmonary superinfections during the
 course of recovery [29,44,45]. Because it is difficult to exclude bacterial infection
as a contributing factor in patients with aspiration, antibiotics are frequently
prescribed at the time of the aspiration event [46]. However, the high rate of
spontaneous recovery from aspiration pneumonitis and observational
comparisons of treated and untreated patients suggest that antibiotics are not
necessary for most patients [47]. In a retrospective review of 200 patients with
aspiration pneumonitis, for example, outcomes were similar for patients
regardless of whether they received empiric antibiotics or not (no difference in
need for intensive care or mortality) [46].
Thus, we reserve use of empiric antibiotics following an aspiration event for
patients who have persistent or progressive respiratory impairment with systemic
signs of inflammation (see 'Choice of regimen' below). In the subset of patients in
whom we do opt to start antibiotics, we re-evaluate the need for continued
antibiotic use after 24, 48, and 72 hours. If pulmonary function and systemic
signs have returned to baseline, we typically stop antibiotics.

BACTERIAL PNEUMONIA
Bacterial aspiration pneumonia is caused by bacteria that normally reside in the
oropharynx or stomach. Historically, aspiration pneumonia has usually referred to an
infection caused by less virulent bacteria, primarily oral anaerobes and streptococci,
which are common constituents of the normal oral flora in patients prone to
aspiration [48]. More recent studies have disputed the dominance of anaerobic
bacteria in aspiration pneumonia, with emphasis on the more common and more
virulent bacteria encountered in hospital-acquired pneumonia and healthcare-
associated pneumonia such as S. aureus, Pseudomonas aeruginosa, and other
aerobic or facultative gram-negative bacilli [6,11-15,49].
These differences in pathogens are best explained by variations in setting
(community, chronic care facility, or hospital), presentation (acute versus subacute
onset), sampling method to avoid upper airway specimen contamination
(transtracheal aspiration, protected brush catheter, or transthoracic aspiration versus
expectorated sputum or routine bronchoscopy), specimen handling, quality of the
microbiologic testing, and prior use of antimicrobials. Sputum specimens from
patients with hospital-acquired pneumonia, even transtracheal aspiration specimens
processed in specialized labs, show high yields of aerobic pathogens, only sometimes
accompanied by obligate anaerobes [50]. It also appears that the late sequelae of
anaerobic lung infections, such as lung abscess, necrotizing pneumonia, and
empyema, are less common than they were in the past for unknown reasons.
Pathophysiology — The standard teaching has been that the lower respiratory tract
is normally sterile below the larynx so that specimens collected in such a way as to
avoid contaminants from above the larynx (transtracheal aspiration, transthoracic
aspiration, bronchoscopy with a protected brush) define pathology. However, more
recent studies using culture-independent molecular techniques have shown that
there is a respiratory tract microbiome that extends from the nasal passages to the
alveoli [51-53]. One possible hypothesis is that people are continually or frequently
“micro-aspirating” leading to new and repeated inoculations [4]. Bacterial aspiration
pneumonia may result from larger inocula, greater pathogenicity of the aspirated
microbes, local and/or systemic impairments in host defenses, or some combination
of these.
Microbiology — Anaerobic bacteria were historically believed to be the dominant
organisms in aspiration pneumonia and its sequelae (lung abscess and empyema),
but subsequent studies suggest that aerobic bacteria are probably at least as
common and clinically important.
The role of anaerobes was identified in the 1970s in studies employing careful
microbiologic techniques for the isolation of anaerobes [2,54-63]. Specimens for
anaerobic culture were carefully obtained from the lower airways without
contamination by upper airway bacteria by using transtracheal aspiration, flexible
bronchoscopy with a shielded brush, transthoracic needle aspiration, or
thoracentesis.
The major anaerobes isolated from pulmonary infections are Peptostreptococcus
(gram-positive cocci in chains), Fusobacterium nucleatum (fusiform gram-negative
bacilli), Fusobacterium necrophorum (long gram-negative bacilli), Prevotella,
Bacteroides melaninogenicus (delicate gram-negative bacilli), and other Bacteroides
spp [54-58].
Subsequent studies of aspiration pneumonias have found that aerobic bacteria may
be more prevalent than anaerobic bacteria, particularly in patients without abscess
formation, and mixed aerobic-anaerobic infections are common, as demonstrated by
the following studies:
● A prospective study of 95 patients from a long-term care facility admitted to an
intensive care unit with pneumonia and risk factors for aspiration found that
gram-negative bacilli were the most common isolates (49 percent), followed by
anaerobic bacteria (16 percent) and S. aureus (12 percent) [11]. Anaerobic
bacteria were accompanied by aerobic gram-negative bacilli in 55 percent of
patients with anaerobic isolates.
● In 212 Japanese patients with lung abscess, streptococci were the most common
pathogens (60 percent of patients) and anaerobes were the second most
common (26 percent) [64].
● Anaerobes appear to be even less common among patients with hospital-
acquired aspiration pneumonia, where Streptococci, S. aureus, and gram-
negative bacilli predominate [6,11-15,65].
Possible explanations for the higher rate of anaerobic infection in older studies
include the assiduous culture techniques that were used, the presentation of patients
later in the disease course, less baseline use of antibiotics with anaerobic activity, and
differences in the oropharyngeal microflora between otherwise healthy community
dwelling and hospitalized adults [52,57,64,66,67].
Clinical features — The presenting findings in bacterial aspiration pneumonia are
highly variable, depending upon when a patient is seen in the course of their
infection, the bacteria involved, and the status of the host. Compared with most cases
of community-acquired pneumonia, aspiration pneumonia involving anaerobes often
evolves slowly. Fever is common; rigors and chills are not. There is usually an
association with periodontal disease, and this complication is less common in patients
with good dental hygiene and those who are edentulous. Hospital-acquired aspiration
pneumonia often involves S. aureus or gram-negative bacilli, which commonly
colonize the oral cavity of hospitalized patients.
Most patients present with the common manifestations of pneumonia, including
cough, fever, purulent sputum, and dyspnea [56]. Cases involving anaerobes usually
evolve over a period of several days or weeks instead of hours [54,55]. Many patients
have accompanying weight loss and anemia as common features of a more chronic
process. With infections involving S. aureus or gram-negative bacilli, the tempo is
much faster.
Clinical features, which are characteristic of bacterial aspiration pneumonia include:
● Indolent onset of symptoms; absence of rigors.
● A predisposing condition for aspiration, usually compromised consciousness due
to substance use disorder, alcoholism, neurologic disease, or anesthesia; or
dysphagia.
● Concurrent evidence of periodontal disease.
● Sputum that has a putrid odor; this finding is often considered diagnostic of
anaerobic infection, although evidence of anaerobic infection does not exclude
the presence of clinically important aerobic pathogens.
● Failure to recover likely pulmonary pathogens with cultures of expectorated
sputum in patients with suggestive clinical syndromes may suggest an anaerobic
infection.
● Gram stain of appropriate specimens that show the characteristic morphologic
features of anaerobes in large numbers, preferably in respiratory specimens that
are uncontaminated by the flora of the upper airways. Such cultures may be read
as oral flora. (See 'Microbiology' above.)
● Chest imaging showing involvement of the dependent portions of the lung or
segments, or an obstructed stricture or foreign body. Imaging with evidence of
pulmonary necrosis with lung abscess and/or an empyema is consistent with an
aspiration pneumonia, although not diagnostic of anaerobic infection.
With the slow tempo that characterizes lung infections involving anaerobes, many
patients present later in their course with complications characterized by suppuration
and necrosis, including lung abscess, necrotizing pneumonia, or empyema [54-56].
(See "Lung abscess in adults" and "Epidemiology, clinical presentation, and diagnostic
evaluation of parapneumonic effusion and empyema in adults".)
By contrast, aspiration of a foreign body or tooth or gastric acid tends to be far more
acute in presentation. (See 'Clinical features' above and 'Mechanical obstruction'
below.)
Evaluation — Bacterial aspiration pneumonia is suspected in patients with new or
worsening respiratory impairment after an aspiration event or with risk factors for
aspiration.
● Dysphagia – A history of coughing while eating or drinking is likely to indicate
aspiration, but aspiration may also be silent [68,69]. Evaluation of dysphagia is
described separately. (See "Approach to the evaluation of dysphagia in adults"
and "Oropharyngeal dysphagia: Clinical features, diagnosis, and management"
and "Swallowing disorders and aspiration in palliative care: Assessment and
strategies for management".)
● Microbiologic studies – Microbiologic studies are obtained depending on the
severity of illness, as with community-acquired pneumonia ( table 3). For
patients who are hospitalized with aspiration pneumonia, whether the aspiration
events occurred in the hospital or at home, we obtain blood cultures and sputum
Gram stain and culture at a minimum. We suggest urine streptococcal antigen
testing, sputum (or urine) Legionella testing, and a respiratory virus panel as well,
given the difficulty differentiating pneumonia due to aspiration of gastric or
oropharyngeal secretions alone versus pneumonia due to other causes.
Molecular diagnostic tests for common bacterial and viral pathogens and their
probable resistance profiles may be helpful where available. (See "Epidemiology,
pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-
associated pneumonia in adults", section on 'Diagnosis'.)
For most hospitalized patients who are not critically ill, sputum studies are
generally sufficient for the identification of clinically important aerobic
organisms. Patients who require mechanical ventilation may be candidates for
bronchoscopy to obtain lower airway samples.
 Thoracentesis is generally indicated if parapneumonic pleural fluid is present.
(See "Epidemiology, clinical presentation, and diagnostic evaluation of
parapneumonic effusion and empyema in adults".)
● Procalcitonin – Procalcitonin has not proven useful in determining the presence
of bacterial lung infection after an aspiration event. In a study of 65 intubated
patients with a witnessed aspiration, procalcitonin, measured on days 1 and 3,
did not distinguish patients with positive lower respiratory cultures from those
with negative cultures [70]. (See "Procalcitonin use in lower respiratory tract
infections".)
● Chest imaging – Occasionally the conventional chest radiograph will be negative
early in the course, but chest computed tomography (CT) will identify the
pneumonia [1,71]. Conversely, CT can often exclude the presence of pneumonia
in patients with equivocal signs and symptoms [72,73]. The main roles for CT are
to identify and characterize abscesses, obstructing objects or lesions, and pleural
disease including empyema.
Diagnosis — The diagnosis of bacterial aspiration pneumonia is generally clinical,
based on the risk factors for aspiration, setting (home, hospital, chronic care facility),
presenting clinical features, and chest imaging showing compatible opacities.
Treatment — In contrast with chemical aspiration pneumonitis, antibiotics are
indicated for treatment of symptomatic aspiration pneumonia when bacterial
infection is suspected. The management of complications of aspiration pneumonia,
such as lung abscess and empyema, are discussed separately. (See "Epidemiology,
clinical presentation, and diagnostic evaluation of parapneumonic effusion and
empyema in adults" and "Lung abscess in adults".)
Choice of regimen — Selection of an initial antibiotic regimen for bacterial
aspiration pneumonia depends on the setting in which aspiration occurred
(outpatient or hospital-acquired), clinical suspicion for anaerobic infection, severity of
illness, and presence of antibiotic allergy ( algorithm 1). The initial regimen is
adjusted as needed based on culture results and response to therapy.
● Community-acquired aspiration pneumonia – For patients with a clinical
history that strongly suggests bacterial aspiration pneumonia, for example
patients with dysphagia, altered mental status, compatible imaging (eg,
dependent consolidative or ground glass opacities), and/or clinical signs of
anaerobic pathogens (eg, putrid breath, severe periodontal disease, or dental
caries), we suggest including anaerobic coverage in addition to targeting routine
community acquired pneumonia (CAP) pathogens (eg, S. pneumoniae). This
approach is slightly different from the American Thoracic Society (ATS) and
Infectious Diseases Society of America (IDSA) guidelines, which do not routinely
add coverage for anaerobes in the absence of lung abscess or empyema [74].
When the clinical history does not strongly suggest aspiration over other causes
of CAP, we generally treat with a standard CAP regimen and do not add coverage
for anaerobes ( algorithm 2A-C). Note, however, that treatment regimens with
and without anaerobic coverage for patients with suspected aspiration have not
been compared in large clinical trials. (See "Treatment of community-acquired
pneumonia in adults who require hospitalization" and "Treatment of community-
acquired pneumonia in adults in the outpatient setting".)
The choice of regimen varies with the severity of illness, risk factors for resistant
pathogens, and antibiotic allergies [74]:
• For outpatients with symptomatic community-acquired aspiration pneumonia
and no risk factors for antibiotic resistant pathogens ( table 4), we suggest
oral amoxicillin-clavulanate (typically 875 mg/125 mg twice daily). Dose
adjustment may be needed in patients with impaired kidney function. We do
not usually add coverage for atypical organisms with a macrolide or
doxycycline when aspiration is strongly suspected. Moxifloxacin is an
acceptable alternative for patients who cannot take amoxicillin/clavulanate or
when additional treatment for atypical pathogens is indicated, but it is less
well-studied in aspiration pneumonia.
• For patients with community-acquired aspiration pneumonia who require
hospitalization but are not severely ill, we suggest ampicillin-sulbactam (1.5 to
3 g every six hours for those with normal kidney function). We prefer this
regimen over other regimens due to better anaerobic coverage (ie, for its
activity against beta-lactamase-producing oral anaerobes). However, whether
 better anaerobic coverage leads to improved clinical outcomes is not clear.
Limited data suggest that other regimens may be similarly effective (ie,
ceftriaxone with or without metronidazole or monotherapy with either
moxifloxacin or clindamycin) [65,75-79].
Alternatives for penicillin-allergic patients are discussed below and separately.
(See "Treatment of community-acquired pneumonia in adults who require
hospitalization", section on 'Medical ward' and "Choice of antibiotics in
penicillin-allergic hospitalized patients".)
• For patients who are severely ill with risk factors for resistant gram-negative
organisms, we suggest initiating intravenous therapy with imipenem,
meropenem, or piperacillin-tazobactam; these agents cover virtually all
anaerobes as well as most aerobic gram-negative bacilli (carbapenems more
so than piperacillin-tazobactam). Coverage for methicillin-resistant S. aureus
(MRSA) can be added if the patient has risk factors ( table 4). For patients with
carbapenem-resistant pseudomonas or other highly resistant gram-negative
organisms, regimen selection is usually individualized and based on
susceptibility profiles.(See "Treatment of community-acquired pneumonia in
adults who require hospitalization", section on 'Intensive care unit'.)
• Alternative regimens based upon in vitro activity and limited clinical data are
the combination of metronidazole (500 mg orally or IV three times daily) plus
amoxicillin (500 mg orally three times daily) or penicillin G (1 to 2 million units
IV every 4 to 6 hours) or ceftriaxone (1 to 2 g IV daily).
Metronidazole should not be used alone since monotherapy is associated with
a failure rate of about 50 percent in the treatment of anaerobic
pleuropulmonary infections [80,81]. The presumed reason for the high failure
rates with metronidazole is its lack of activity against streptococci, which can
be cultured in approximately 40 to 70 percent of cases.
● Hospital-acquired or healthcare-associated aspiration pneumonia – For
hospital-acquired or healthcare-associated aspiration pneumonia, aerobic
bacteria, especially gram-negative bacilli and S. aureus, are generally more
important than anaerobes and are usually easily detected from adequate
 specimens [11,50,74]. For most patients, targeting these pathogens according to
the guidelines for hospital acquired pneumonia (HAP) is sufficient ( algorithm 3
and algorithm 4).
However, we add treatment for anaerobes when there is a higher likelihood that
they are involved in the infection (eg, patients with observed or likely aspiration,
concern for dental infection, concomitant lung abscess or empyema, or
persistent clinical deterioration despite treatment against aerobic bacteria). When
there is a perceived need to treat resistant aerobic gram-negative bacilli plus
anaerobes (eg, in patients known to be colonized with resistant gram-negative
bacilli or patients who have received IV antibiotics within the past 90 days), we
suggest a carbapenem (imipenem, meropenem) or piperacillin-tazobactam since
these agents cover virtually all anaerobes as well as most aerobic gram-negative
bacilli (carbapenems more so than piperacillin-tazobactam). Before culture and
susceptibility results are available, patients with risk factors for MRSA (eg, prior
colonization) also require an agent with activity against MRSA (vancomycin or
linezolid), but if MRSA is not detected, then this agent should be discontinued.
The management of hospital-acquired pneumonia is discussed in detail separately.
(See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)
● Penicillin allergy – For out-patients who cannot tolerate penicillin, moxifloxacin
(400 mg, once daily) is an appropriate choice; clindamycin (300 to 450 mg orally
every eight hours) is an alternative, although it carries a greater risk of
Clostridioides difficile infection.
Hospitalized patients who are able to take cephalosporins can take a combination
of either ceftriaxone (1 or 2 g IV daily) or cefotaxime (1 or 2 g IV every 8 hours)
with metronidazole (500 mg every 8 hours). Carbapenems may be a reasonable
alternative for some patients but have a broader spectrum.
Additional information about beta-lactam allergy is provided separately. (See
"Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic
strategies and cross-reactivity with other beta-lactam antibiotics" and "Immediate
cephalosporin hypersensitivity: Allergy evaluation, skin testing, and cross-
reactivity with other beta-lactam antibiotics" and "Treatment of community-
 acquired pneumonia in adults who require hospitalization", section on 'Penicillin
and cephalosporin allergy' and "Treatment of community-acquired pneumonia in
adults who require hospitalization", section on 'Penicillin and cephalosporin
allergy'.)
● Adjusting therapy when culture results are available – When aerobic
pathogens are involved as primary pathogens or copathogens with anaerobes,
the antibiotic regimen should be tailored based upon the respiratory aerobic
culture and susceptibility results. As anaerobic culture and susceptibility results
are often not available in clinical practice, decisions about the selection of
antibiotic coverage for anaerobic copathogens must be made on the basis of
published estimates of current susceptibility patterns.
● Other antibiotics – Moxifloxacin has in vitro activity against respiratory
pathogens including anaerobes, but it has not been adequately studied for
aspiration pneumonia, and some data have suggested increasing rates of
resistance of anaerobes to moxifloxacin. In addition, fluoroquinolones are
associated with a higher risk of C. difficile infection than certain other antibiotic
classes. (See 'Efficacy' below and "Clostridioides difficile infection in adults:
Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)
Other agents commonly employed for pulmonary infections such as macrolides,
tetracyclines, and cephalosporins have not been systematically studied in
aspiration pneumonia.
All of the suggested regimens increase the risk of C. difficile infection, especially in
patients with other risk factors such as hospitalization, advanced age, and severe
illness. (See "Clostridioides difficile infection in adults: Epidemiology, microbiology,
and pathophysiology", section on 'Risk factors'.)
Duration of antibiotics and transition to oral therapy — The duration of
antibiotics for aspiration pneumonia is arbitrary and not well studied. The usual
duration of therapy for cases that are not complicated by cavitation or empyema is
five days for community-acquired aspiration pneumonia and seven days for hospital-
acquired aspiration pneumonia; shorter therapy may be effective but has not been
adequately studied. Patients who are initially treated with parenteral antibiotics can
be switched to oral antibiotics when they are improving clinically, hemodynamically
stable, able to take oral medications, and have a normally functioning gastrointestinal
tract [74]. An appropriate choice for most patients is amoxicillin-clavulanate (875 mg
orally twice daily). For patients who have a serious allergy (eg, an Ig-E mediated
reaction) to penicillin, moxifloxacin (400 mg once daily) or clindamycin (450 mg orally
three times daily) can be given.
Patients with associated pleural effusions should have a thoracentesis to exclude
empyema, which often complicates pneumonia involving anaerobes. Patients with
lung abscess need a longer course of antibiotics, usually until there is radiographic
clearance or significant improvement, leaving only a small stable residual lesion. (See
"Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic
effusion and empyema in adults" and "Lung abscess in adults", section on 'Duration
of antibiotics'.)
As some patients initially thought to have aspiration pneumonia actually have
chemical pneumonitis, it is appropriate to discontinue antibiotics if the signs and
symptoms of pneumonia rapidly resolve.
Efficacy — Several regimens have been found to be effective in bacterial aspiration
pneumonia, including ampicillin-sulbactam, amoxicillin-clavulanate, moxifloxacin,
clindamycin, imipenem, ceftriaxone, and penicillin with metronidazole.
● A randomized trial evaluated the efficacy of clindamycin (600 mg twice daily),
ampicillin-sulbactam (half dose, 1.5 g twice daily), ampicillin-sulbactam (full dose,
3 g twice daily), or imipenem (500 mg twice daily) in 100 older adult patients with
aspiration pneumonia [77]. All regimens were equally effective (cure rates ranged
from 76 to 88 percent), but clindamycin was associated with a lower rate of
posttreatment occurrence of methicillin-resistant S. aureus superinfection (0 of 25
compared with 5 to 8 of 25 in the other treatment arms). Diarrhea was not
reported as an adverse effect in the clindamycin group, although it is known to be
associated with C. difficile diarrhea.
● In an open-label, randomized trial that compared ampicillin-sulbactam with
moxifloxacin in 96 patients with aspiration pneumonia or lung abscess, clinical
resolution was noted in 66.7 percent of both groups [65]. While this trial found
 that clinical cure rates with moxifloxacin were comparable to ampicillin-
sulbactam, it has not been studied adequately to recommend it as a first-line
agent for aspiration pneumonia, and the rate of resistance of anaerobes to this
drug is increasing [78].
● Alternative regimens that appear effective include amoxicillin-clavulanate
(studied in lung abscess) [82] and penicillin combined with metronidazole [79]. As
noted above, metronidazole should not be used alone but can be used if
combined with a beta-lactam antibiotic.
● Clindamycin is superior to penicillin alone in the treatment of necrotizing
pneumonia and putrid lung abscess in terms of response rates and time to
defervescence [83,84]. In one study of 37 patients with lung abscess or
necrotizing pneumonia, the failure rate with clindamycin was 15 percent versus
44 percent with penicillin alone [84].
● Three retrospective propensity-matched analyses suggest regimens with limited
anaerobic coverage (eg, ceftriaxone) may be associated with similar cure rates
compared with regimens with extended anaerobic coverage (eg, ceftriaxone plus
metronidazole or moxifloxacin or an extended-spectrum penicillin).
- In one multicenter study of community-acquired aspiration pneumonia
requiring hospitalization, over 1300 patients who mostly received
ceftriaxone plus metronidazole or moxifloxacin were compared with nearly
2700 patients receiving ceftriaxone alone or other regimens with limited
anaerobic coverage [85]. After propensity matching, extended coverage did
not improve mortality (32.1 versus 30.3 percent, adjusted risk difference 1.6
percent increase in mortality in the extended coverage group; 95% CI –1.7
to 4.9). There was a small but significant increase in rates of Clostridium
difficile colitis in the extended anaerobic coverage group (0.8-1.1 percent
versus ≤0.2 percent, adjusted risk difference 1.0 percent, 95% CI 0.3-1.7).
- In a separate study, 218 patients treated with ceftriaxone were matched to
218 patients treated with ampicillin-sulbactam using propensity scores [76].
There was no significant difference in mortality rates (HR 0.80, 95% CI 0.41-
1.58). Ceftriaxone was associated with significantly more hospital-free days
 compared with ampicillin-sulbactam (11 days, 95% CI 10-13 versus 9 days,
95% CI 8-10).
- A smaller study matched 23 patients treated with ceftriaxone to 23 patients
treated with piperacillin-tazobactam or a carbapenem and found no
difference in 30-day mortality or hospital length of stay [75].
These trials all suffer from considerable heterogeneity in the diagnosis of
aspiration pneumonia and may include patients with aspiration pneumonitis or
community-acquired pneumonia without significant aspiration. The inclusion
of patients who do not clearly have aspiration pneumonia may dilute study
results and make it more difficult to detect an effect of different treatment
regimens on aspiration pneumonia in particular. In addition, despite
propensity matching, there may also be some residual confounding based on
clinical judgment. These issues decrease our certainty in the findings above.
The benefit of extended coverage is probably greatest in those with large
volume aspiration, including witnessed emesis, delayed diagnosis, CT evidence
of cavitation in dependent lung segments, and/or putrid breath. Given the
persistent uncertainties in published studies on the treatment of aspiration
pneumonia, we continue to favor adding directed anaerobic coverage for these
groups.
Outcomes — The cure rate for aspiration pneumonia with antibiotic therapy is 76 to
88 percent [77]. Long-term follow-up studies of patients who survive severe aspiration
pneumonia have revealed complete recovery in some patients and radiographic
evidence of pulmonary fibrosis in others ( image 3) [86,87].

MECHANICAL OBSTRUCTION
Aspiration pneumonia may involve fluid or particulate matter, which are not
inherently toxic to the lung but can cause airway obstruction or reflex airway closure
( image 4).
Fluids — Typical fluids that are aspirated and are not intrinsically toxic to the lungs
include:
 ● Saline
● Barium ( image 5)

● Most ingested fluids including water

● Gastric contents with a pH exceeding 2.5

The most frequently observed form of fluid aspiration causing simple mechanical
obstruction is that noted in victims of drowning. Patients at risk for mechanical
obstruction are those who cannot clear the inoculum due to a profound neurologic
deficit such as absence of a cough reflex or impaired consciousness.
Witnessed aspiration is treated with lateral head positioning and oropharyngeal
suctioning; tracheal suctioning is performed if an endotracheal tube is in place. If the
patient rapidly recovers or subsequent chest radiograph does not show a new
pulmonary opacity, no further therapy is required except for measures intended to
prevent subsequent episodes of aspiration. In hospitalized patients, the most
important preventive measure is semi-upright or upright positioning, particularly
during feeding [88]. (See 'Prevention' below.)
Solid particle aspiration — The severity of respiratory obstruction depends upon the
relative size of the object that is aspirated and the caliber of the lower airways.
Foreign body aspiration is most common in children from one to three years of age
and among older adults [89]. The usual objects recovered from the lower airways are
peanuts, other vegetable particles, inorganic materials, and teeth [90-93]. Vegetable
materials, including peanuts, are problematic because they are not visualized on plain
chest radiographs. (See "Airway foreign bodies in adults".)
The clinical consequences depend upon the level of obstruction. Large objects that
lodge in the larynx or trachea cause sudden respiratory distress, cyanosis, and
aphonia that lead quickly to death if the obstruction is not immediately reversed. This
is sometimes referred to as the "café coronary syndrome" because the symptoms
simulate those of myocardial infarction and are often seen with aspiration of meat
during restaurant dining [94]. The suggested treatment is the Heimlich maneuver
consisting of firm and rapid pressure applied to the upper abdomen in an effort to
force the diaphragm up to dislodge the particle.
Aspiration of smaller particles causes less severe obstruction. These patients often
present with an irritative cough, and chest radiograph shows atelectasis or
obstructive emphysema with a cardiac shift and elevated diaphragm. When the
obstruction is partial, unilateral wheezing may be appreciated.
For patients who are not able to expectorate particulate matter, the primary
therapeutic modality is removal of the foreign object, usually with flexible or rigid
bronchoscopy [95]. Bacterial superinfection is a frequent complication when the
obstruction or partial obstruction persists for more than one week [96,97]; the usual
pathogens are anaerobic bacteria from the upper airways as described above. (See
"Airway foreign bodies in adults".)

LIPOID PNEUMONIA
Exogenous lipoid pneumonia is most commonly caused by the aspiration of mineral
oil when ingested to treat constipation or used intranasally as a vehicle for
decongestants or as a home remedy for nasal dryness [98-101]; other causes include
aspiration of industrial oils and nasal application of white petrolatum [102,103]. The
most commonly affected patients are those at the extremes of age who have risk
factors for aspiration. The result is either an inflammatory response with regional
edema and intraalveolar hemorrhage or a "paraffinoma" with aspirated oils
encapsulated by fibrous tissue ( image 6) [102,104,105].
It has been hypothesized that exogenous lipoid pneumonia may be precipitated in
some patients with e-cigarette or vaping product use associated lung injury (EVALI),
due to the inhalation of heated oils as some investigators have noted lipid-laden
macrophages in the bronchoalveolar lavage of some patients. (See "E-cigarette or
vaping product use-associated lung injury (EVALI)", section on 'Pathogenesis and risk
factors'.)
Some patients (usually children) have an acute inflammatory reaction to oil aspiration
and present acutely with cough, fever, and dyspnea. Other patients (usually older
adults) have recurrent, asymptomatic events and are identified because of an
abnormality noted on chest radiograph or present with a chronic cough, sometimes
with sputum production, and dyspnea [98]. Chest pain, hemoptysis, weight loss, and
fever are less common. The chest radiograph typically reveals bilateral lower lung
zone opacities that may be poorly-defined or mass-like [98,106].
The diagnosis of exogenous lipoid pneumonia is largely based on chest computed
tomography (CT) findings, supported by a compatible history of exposure and
bronchoalveolar lavage. Chest CT findings are often more extensive than expected
based on symptoms and include ground glass opacities, thickened interlobular septa,
crazy paving, and air bronchograms ( image 6) [98,104]. Areas of consolidation
containing foci of fat attenuation (<-30 Hounsfield units) are a characteristic feature
[98,107].
Bronchoalveolar lavage (BAL) is often performed to evaluate for infection and
malignancy. In lipoid pneumonia, BAL may reveal lipid-laden macrophages with large
vacuoles that stain positive with Oil-Red-O stain, although this finding is nonspecific
and may be falsely negative [98,108].
Treatment of exogenous lipoid pneumonia focuses on cessation of exposure to the oil
source [99,106,109]. Many patients have sufficient improvement with avoidance that
further therapy is not needed. For patients with more severe disease, a trial of
systemic glucocorticoids may be a reasonable option, although the response has
been mixed in observational studies [106,109-111]. For patients with severe
respiratory impairment that is refractory to exposure cessation and a trial of systemic
glucocorticoids, a few case reports describe improvement with whole lung lavage in
patients with extensive lipoid pneumonia and severe respiratory impairment
[109,111-113]. Whole lung lavage is used in pulmonary alveolar proteinosis and
should only be undertaken in centers with experience in this technique. (See
"Treatment and prognosis of pulmonary alveolar proteinosis in adults", section on
'Whole lung lavage'.)

PREVENTION
A number of interventions have been proposed to prevent aspiration, especially in
older adult patients and stroke patients, although supportive data are limited:
● Semi-recumbent position – Data are mixed regarding the efficacy of a semi-
recumbent (eg, 30 to 45 degree) position for preventing aspiration events
[114,115], although we are in favor of using the semi-recumbent position for
patients receiving enteral nutrition and those with reduced mental status.
● Enteral feeding – Percutaneous gastrostomy tubes and nasogastric tubes are
efficient for delivering nutrition and oral medications in patients with dysphagia,
but have not been shown to reduce the incidence of aspiration pneumonia
compared with oral feeding [6,116,117]. Postpyloric tubes (eg, nasoduodenal,
jejunal) may reduce aspiration compared with gastric tubes [118].
● Speech and swallowing evaluation – For patients with impaired swallowing,
particularly after stroke or intubation/mechanical ventilation, a full speech and
swallowing evaluation is prudent. When a full evaluation is not possible, a water
swallow test may help identify patients at increased risk of aspiration, although
the test has a high false positive rate. (See "Oropharyngeal dysphagia: Clinical
features, diagnosis, and management" and "Complications of stroke: An
overview", section on 'Dysphagia'.)
● Thickened liquids and chin-down position – Thickened liquids may improve
swallowing safety, but with the consequence of increased dehydration and
reduced palatability and quality of life [1,119,120]. A potentially less effective
alternative that patients may prefer is maintaining a chin-down position when
swallowing liquids. A randomized trial compared chin-down position and oral
feedings of two consistencies (nectar thickened or honey thickened) on the
incidence of aspiration as assessed by videofluorography in 711 patients with
dementia or Parkinson disease [121]. Significantly more patients aspirated on
thin liquids using the chin-down posture (68 percent) than when using nectar-
thickened liquids (63 percent) or honey-thickened liquids (53 percent). However, a
separate report evaluating the incidence of pneumonia at three months in a
subset of 515 patients found no significant difference between patients
randomized to chin-down position versus thickened liquids (9.8 versus 11.6
percent) [122]. There was no control group, so one cannot determine if the
interventions were effective compared with no intervention. There were
numerically more episodes of the combined outcome of dehydration, urinary
 tract infection, and fever amongst patients randomized to thickened liquids (9
versus 5 percent, p = 0.055).
● Nausea and dysphagia control – Prokinetics have been associated with lower
rates of pneumonia in stroke patients. In one study, 60 patients within seven days
of an acute stroke who required nasogastric tubes were randomized to daily
metoclopramide versus placebo. Use of metoclopramide was associated with
significantly lower rates of aspiration and pneumonia (27 versus 87 percent)
[123]. In another placebo-controlled trial of 150 patients with acute ischemic
stroke, daily administration of domperidone was associated with significantly less
dysphagia, nausea and vomiting, and aspiration pneumonia [124].
● Multicomponent strategy – A cluster randomized trial sought to determine
whether a multicomponent strategy (including manual tooth/gum brushing plus
0.12 percent chlorhexidine oral rinse twice daily plus upright positioning during
feeding) could reduce the incidence of pneumonia amongst 834 nursing home
residents compared with usual care. The investigators found no significant
difference in pneumonia rates in the intervention versus control arms (27.4
versus 23.5 percent) [125]. It might have been difficult to detect a difference
between the groups since upright positioning during feeding is practiced
routinely in nursing homes [126], and oral hygiene is also a common part of usual
nursing home care. However, a second cluster randomized trial amongst 2152
nursing home residents that focused on improving residents’ oral hygiene by
improving staff members’ knowledge, attitudes, and practical skills in performing
oral hygiene similarly found no difference in pneumonia rates over a two-year
period (0.67 versus 0.72 pneumonias per 1000 resident-days) [127].
Techniques for the prevention of aspiration in hospitalized patients are discussed
separately. (See "Risk factors and prevention of hospital-acquired and ventilator-
associated pneumonia in adults".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and
regions around the world are provided separately. (See "Society guideline links:
Community-acquired pneumonia in adults".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond
the Basics." The Basics patient education pieces are written in plain language, at the
5th to 6th grade reading level, and they answer the four or five key questions a patient
might have about a given condition. These articles are best for patients who want a
general overview and who prefer short, easy-to-read materials. Beyond the Basics
patient education pieces are longer, more sophisticated, and more detailed. These
articles are written at the 10th to 12th grade reading level and are best for patients
who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage
you to print or email these topics to your patients. (You can also locate patient
education articles on a variety of subjects by searching on "patient info" and the
keyword(s) of interest.)
● Basics topic (see "Patient education: Aspiration pneumonia (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Definition – Aspiration pneumonia refers to the adverse pulmonary
consequences that can sometimes result from aspiration of fluid, particulate
exogenous substances, or endogenous secretions into the lower airways. (See
'Introduction' above and 'Definitions' above.)
● Aspiration syndromes – Syndromes commonly associated with aspiration
include:
• Chemical pneumonitis, which refers to the aspiration of substances (eg, acidic
gastric fluid) that cause an inflammatory reaction in the lower airways,
independent of bacterial infection. (See 'Chemical pneumonitis' above.)
• Bacterial aspiration pneumonia, which refers to infection that results from
inoculation of orogastric contents and bacteria. (See 'Bacterial pneumonia'
 above.)
• Mechanical obstruction, which refers to aspiration of fluid or particulate
matter that leads to airway obstruction or triggers reflex airway closure. (See
'Mechanical obstruction' above.)
• These syndromes are not mutually exclusive and thus it can be challenging to
classify individual cases. Understanding the risk factors for aspiration and the
pathophysiology that underlies each of these syndromes can help guide care.
(See 'Predisposing conditions' above.)
● Immediate treatment following aspiration
• All patients with an observed aspiration should have immediate pharyngeal or
tracheal suction to clear fluids and particulate matter that may cause
obstruction. (See 'Treatment' above.)
• Antimicrobial agents should be given following a witnessed aspiration in
patients who develop new and persistent impaired oxygenation with
associated inflammatory findings. Antibiotics are not necessary in patients that
aspirate but rapidly recover. (See 'Treatment' above.)
● Considerations regarding anaerobic coverage – While anaerobes have
traditionally been implicated in aspiration pneumonia, more recent data suggest
aerobic bacteria predominate. Thus, it can be difficult to determine when to
include an agent that targets anaerobes in the initial empiric treatment regimen.
In general, we make this determination based on the degree of suspicion for
aspiration, the clinical setting (community versus hospital-acquired), the severity
of illness, and the patient’s clinical trajectory. (See 'Microbiology' above and
'Treatment' above.)
● Treatment recommendations for community-acquired aspiration pneumonia
– For patients with a clinical picture that is strongly suggestive of aspiration
pneumonia acquired in a community setting (eg, witnessed aspiration event, risk
factors for aspiration, compatible imaging, subacute course, putrid breath), we
select an antibiotic regimen that includes coverage for most pathogenic oral
flora, including anaerobic bacteria. The specific regimen varies with the clinical
 setting, severity of illness, risk factors for resistant pathogens, and antibiotic
allergies ( algorithm 1) (see 'Choice of regimen' above):
• For outpatients, we suggest amoxicillin-clavulanate (typically, 875 mg/125 mg
twice daily) (Grade 2C), with dose adjustments as needed for gastrointestinal
intolerance or kidney impairment. We do not usually add a macrolide or
doxycycline when aspiration is strongly suspected. Moxifloxacin is an
acceptable alternative for patients who cannot take amoxicillin/clavulanate or
when additional treatment for atypical pathogens is indicated, but it is less
well-studied in aspiration pneumonia. Clindamycin (300 to 450 mg orally every
eight hours) is an additional alternative, although it carries a greater risk of
Clostridioides difficile infection.
• For patients who require hospitalization but are not severely ill, we suggest
ampicillin-sulbactam (1.5–3 g every six hours for those with normal kidney
function) rather than other regimens due to better anaerobic coverage (Grade
2C). Modifications to the regimen may be needed for patients who are severely
ill or have risk factors for Pseudomonas, methicillin resistant Staphylococcus
aureus (MRSA), or other drug resistant pathogens ( table 4).
● Treatment recommendations for hospital-acquired aspiration pneumonia –
For patients with aspiration pneumonia acquired in a hospital setting, we
generally target aerobic bacteria, because they are generally more important
than anaerobes, using standard hospital acquired pneumonia (HAP) algorithms
( algorithm 3 and algorithm 4). However, for patients with a witnessed
aspiration, severe periodontal disease, imaging suggesting a necrotizing process,
or failure to respond to an antibiotic regimen without anaerobic coverage, we
add anaerobic coverage.
• Reasonable choices for most patients include imipenem, meropenem, or
piperacillin-tazobactam. Modifications may be needed for patients with risk
factors or evidence of MRSA or other resistant pathogens ( table 4). (See
'Choice of regimen' above.)
• For hospitalized patients who have a serious penicillin allergy (eg, an IgE-
mediated reaction) and suspected anaerobic infection, potential alternatives
 include either a combination of a third, fourth, or fifth generation
cephalosporin plus metronidazole (500 mg three times daily) or a
carbapenem, depending on the type and severity of reactions to beta-lactams.
Metronidazole is preferred over clindamycin in combination regimens because
of concern for C. difficile, but metronidazole should not be used as
monotherapy. (See 'Choice of regimen' above.)
● Duration of antibiotics and transition to oral therapy
• Patients who are initially treated with parenteral antibiotics can be switched to
oral antibiotics when they are improving clinically, hemodynamically stable,
able to take oral medications, and have a normally functioning gastrointestinal
tract. For most such patients, we advise amoxicillin-clavulanate (875 mg orally
twice daily). (See 'Duration of antibiotics and transition to oral therapy' above.)
• The duration of antibiotics for aspiration pneumonia is arbitrary and not well
studied. The usual duration of therapy for cases that are not complicated by
cavitation or empyema is five days for community acquired aspiration
pneumonia and seven days for hospital acquired aspiration pneumonia. As
some patients initially thought to have aspiration pneumonia actually have
chemical pneumonitis, it is appropriate to discontinue antibiotics if the
patient’s signs and symptoms of pneumonia rapidly resolve. (See 'Duration of
antibiotics and transition to oral therapy' above.)
● Mechanical obstruction – Aspiration events may involve fluid or particulate
matter ( image 4), which are not inherently toxic to the lung but can cause
airway obstruction or reflex airway closure. If the patient is not able to
expectorate particulate matter, the primary therapeutic modality is removal with
flexible or rigid bronchoscopy. (See 'Mechanical obstruction' above.)
● Lipoid pneumonia – Exogenous lipoid pneumonia is most commonly caused by
the aspiration of mineral oil, industrial oils, or white petrolatum when ingested or
applied intranasally and subsequently aspirated. The diagnosis may be based on
chest computed tomography; common features include ground glass opacities,
thickened interlobular septa, crazy paving, air bronchograms, and areas of
consolidation containing foci of fat attenuation. (See 'Lipoid pneumonia' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate acknowledge John G Bartlett, MD, who contributed to
earlier versions of this topic review.
REFERENCES

1. Mandell LA, Niederman MS. Aspiration Pneumonia. N Engl J Med 2019; 380:651.
2. Bartlett JG, Gorbach SL. The triple threat of aspiration pneumonia. Chest 1975;
68:560.
3. Taylor JK, Fleming GB, Singanayagam A, et al. Risk factors for aspiration in
community-acquired pneumonia: analysis of a hospitalized UK cohort. Am J Med
2013; 126:995.
4. Jaillette E, Girault C, Brunin G, et al. Impact of tapered-cuff tracheal tube on
microaspiration of gastric contents in intubated critically ill patients: a multicenter
cluster-randomized cross-over controlled trial. Intensive Care Med 2017; 43:1562.
5. Torres A, Serra-Batlles J, Ros E, et al. Pulmonary aspiration of gastric contents in
patients receiving mechanical ventilation: the effect of body position. Ann Intern
Med 1992; 116:540.
6. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001;
344:665.
7. BERSON W, ADRIANI J. Silent regurgitation and aspiration during anesthesia.
Anesthesiology 1954; 15:644.
8. Huxley EJ, Viroslav J, Gray WR, Pierce AK. Pharyngeal aspiration in normal adults
and patients with depressed consciousness. Am J Med 1978; 64:564.
9. Lo WL, Leu HB, Yang MC, et al. Dysphagia and risk of aspiration pneumonia: A
nonrandomized, pair-matched cohort study. J Dent Sci 2019; 14:241.
10. Herzig SJ, LaSalvia MT, Naidus E, et al. Antipsychotics and the Risk of Aspiration
Pneumonia in Individuals Hospitalized for Nonpsychiatric Conditions: A Cohort
Study. J Am Geriatr Soc 2017; 65:2580.
11. El-Solh AA, Pietrantoni C, Bhat A, et al. Microbiology of severe aspiration
pneumonia in institutionalized elderly. Am J Respir Crit Care Med 2003; 167:1650.
12. Mier L, Dreyfuss D, Darchy B, et al. Is penicillin G an adequate initial treatment for
aspiration pneumonia? A prospective evaluation using a protected specimen
brush and quantitative cultures. Intensive Care Med 1993; 19:279.
13. Polverino E, Dambrava P, Cillóniz C, et al. Nursing home-acquired pneumonia: a 10
year single-centre experience. Thorax 2010; 65:354.
14. Carratalà J, Mykietiuk A, Fernández-Sabé N, et al. Health care-associated
pneumonia requiring hospital admission: epidemiology, antibiotic therapy, and
clinical outcomes. Arch Intern Med 2007; 167:1393.
15. Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated
pneumonia and aspiration pneumonia: a prospective study. Chest 1999; 115:178.
16. Vieira Colombo AP, Magalhães CB, Hartenbach FA, et al. Periodontal-disease-
associated biofilm: A reservoir for pathogens of medical importance. Microb
Pathog 2016; 94:27.
17. Terpenning MS, Taylor GW, Lopatin DE, et al. Aspiration pneumonia: dental and
oral risk factors in an older veteran population. J Am Geriatr Soc 2001; 49:557.
18. Muder RR. Pneumonia in residents of long-term care facilities: epidemiology,
etiology, management, and prevention. Am J Med 1998; 105:319.
19. Makhnevich A, Feldhamer KH, Kast CL, Sinvani L. Aspiration Pneumonia in Older
Adults. J Hosp Med 2019; 14:429.
20. DiBardino DM, Wunderink RG. Aspiration pneumonia: a review of modern trends. J
Crit Care 2015; 30:40.
21. Perbet S, Mongardon N, Dumas F, et al. Early-onset pneumonia after cardiac
arrest: characteristics, risk factors and influence on prognosis. Am J Respir Crit
Care Med 2011; 184:1048.
22. François B, Cariou A, Clere-Jehl R, et al. Prevention of Early Ventilator-Associated
Pneumonia after Cardiac Arrest. N Engl J Med 2019; 381:1831.
23. Cook D, Deane A, Lauzier F, et al. Stress Ulcer Prophylaxis during Invasive
Mechanical Ventilation. N Engl J Med 2024; 391:9.
24. Wang Y, Parpia S, Ge L, et al. Proton-Pump Inhibitors to Prevent Gastrointestinal
Bleeding - An Updated Meta-Analysis. NEJM Evid 2024; 3:EVIDoa2400134.
25. Krag M, Marker S, Perner A, et al. Pantoprazole in Patients at Risk for
Gastrointestinal Bleeding in the ICU. N Engl J Med 2018; 379:2199.
26. Reza Shariatzadeh M, Huang JQ, Marrie TJ. Differences in the features of aspiration
pneumonia according to site of acquisition: community or continuing care facility.
J Am Geriatr Soc 2006; 54:296.
27. Cabre M, Serra-Prat M, Palomera E, et al. Prevalence and prognostic implications
of dysphagia in elderly patients with pneumonia. Age Ageing 2010; 39:39.
28. MENDELSON CL. The aspiration of stomach contents into the lungs during
obstetric anesthesia. Am J Obstet Gynecol 1946; 52:191.
29. Bynum LJ, Pierce AK. Pulmonary aspiration of gastric contents. Am Rev Respir Dis
1976; 114:1129.
30. Doyle RL, Szaflarski N, Modin GW, et al. Identification of patients with acute lung
injury. Predictors of mortality. Am J Respir Crit Care Med 1995; 152:1818.
31. TEABEAUT JR 2nd. Aspiration of gastric contents; an experimental study. Am J
Pathol 1952; 28:51.
32. Fisk RL, Symes JF, Aldridge LL, Couves CM. The pathophysiology and experimental
therapy of acid pneumonitis in ex vivo lungs. Chest 1970; 57:364.
33. Cameron JL, Caldini P, Toung JK, Zuidema GD. Aspiration pneumonia: physiologic
data following experimental aspiration. Surgery 1972; 72:238.
34. Mays EE, Dubois JJ, Hamilton GB. Pulmonary fibrosis associated with
tracheobronchial aspiration. A study of the frequency of hiatal hernia and
gastroesophageal reflux in interstitial pulmonary fibrosis of obscure etiology.
Chest 1976; 69:512.
35. Johnson LF, Rajagopal KR. Aspiration resulting from gastroesophageal reflux. A
cause of chronic bronchopulmonary disease. Chest 1988; 93:676.
36. Goldman G, Welbourn R, Kobzik L, et al. Tumor necrosis factor-alpha mediates
acid aspiration-induced systemic organ injury. Ann Surg 1990; 212:513.
37. Folkesson HG, Matthay MA, Hébert CA, Broaddus VC. Acid aspiration-induced lung
injury in rabbits is mediated by interleukin-8-dependent mechanisms. J Clin Invest
1995; 96:107.
38. Yamada H, Kudoh I, Nishizawa H, et al. Complement partially mediates acid
aspiration-induced remote organ injury in the rat. Acta Anaesthesiol Scand 1997;
41:713.
39. Wu YC, Hsu PK, Su KC, et al. Bile acid aspiration in suspected ventilator-associated
pneumonia. Chest 2009; 136:118.
40. DePaso WJ. Aspiration pneumonia. Clin Chest Med 1991; 12:269.
41. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration
during the perioperative period. Anesthesiology 1993; 78:56.
42. Raghavendran K, Nemzek J, Napolitano LM, Knight PR. Aspiration-induced lung
injury. Crit Care Med 2011; 39:818.
43. Wolfe JE, Bone RC, Ruth WE. Effects of corticosteroids in the treatment of patients
with gastric aspiration. Am J Med 1977; 63:719.
44. Cameron JL, Mitchell WH, Zuidema GD. Aspiration pneumonia. Clinical outcome
following documented aspiration. Arch Surg 1973; 106:49.
45. Dines DE, Titus JL, Sessler AD. Aspiration pneumonitis. Mayo Clin Proc 1970;
45:347.
46. Dragan V, Wei Y, Elligsen M, et al. Prophylactic Antimicrobial Therapy for Acute
Aspiration Pneumonitis. Clin Infect Dis 2018; 67:513.
47. Jaoude P, Badlam J, Anandam A, El-Solh AA. A comparison between time to clinical
stability in community-acquired aspiration pneumonia and community-acquired
pneumonia. Intern Emerg Med 2014; 9:143.
48. Bartlett JG. How important are anaerobic bacteria in aspiration pneumonia: when
should they be treated and what is optimal therapy. Infect Dis Clin North Am 2013;
27:149.
49. Marin-Corral J, Pascual-Guardia S, Amati F, et al. Aspiration Risk Factors,
Microbiology, and Empiric Antibiotics for Patients Hospitalized With Community-
Acquired Pneumonia. Chest 2021; 159:58.
50. Bartlett JG, O'Keefe P, Tally FP, et al. Bacteriology of hospital-acquired pneumonia.
Arch Intern Med 1986; 146:868.
51. Dickson RP, Erb-Downward JR, Huffnagle GB. The role of the bacterial microbiome
in lung disease. Expert Rev Respir Med 2013; 7:245.
52. Bassis CM, Erb-Downward JR, Dickson RP, et al. Analysis of the upper respiratory
tract microbiotas as the source of the lung and gastric microbiotas in healthy
individuals. MBio 2015; 6:e00037.
53. Dickson RP, Erb-Downward JR, Martinez FJ, Huffnagle GB. The Microbiome and the
Respiratory Tract. Annu Rev Physiol 2016; 78:481.
54. Bartlett JG. Anaerobic bacterial infections of the lung and pleural space. Clin Infect
Dis 1993; 16 Suppl 4:S248.
55. Finegold SM. Aspiration pneumonia. Rev Infect Dis 1991; 13 Suppl 9:S737.
56. Bartlett JG. Anaerobic bacterial pneumonitis. Am Rev Respir Dis 1979; 119:19.
57. Lorber B, Swenson RM. Bacteriology of aspiration pneumonia. A prospective study
of community- and hospital-acquired cases. Ann Intern Med 1974; 81:329.
58. Finegold SM, George WL, Mulligan ME. Anaerobic infections. Part II. Dis Mon 1985;
31:1.
59. Yamashita Y, Kohno S, Tanaka K, et al. [Anaerobic respiratory infection--evaluation
of methods of obtaining specimens]. Kansenshogaku Zasshi 1994; 68:631.
60. Bartlett JG. Diagnostic accuracy of transtracheal aspiration bacteriologic studies.
Am Rev Respir Dis 1977; 115:777.
61. Bordelon JY Jr, Legrand P, Gewin WC, Sanders CV. The telescoping plugged
catheter in suspected anaerobic infections. A controlled series. Am Rev Respir Dis
1983; 128:465.
62. Bartlett JG, Alexander J, Mayhew J, et al. Should fiberoptic bronchoscopy aspirates
be cultured? Am Rev Respir Dis 1976; 114:73.
63. Fletcher EC, Mohr JA, Levin DC, Flournoy DJ. Bronchoscopic diagnosis of
pulmonary infections. Comparison of protected-specimen brush and cytology
brush with lung aspirates. West J Med 1983; 138:364.
64. Takayanagi N, Kagiyama N, Ishiguro T, et al. Etiology and outcome of community-
acquired lung abscess. Respiration 2010; 80:98.
65. Ott SR, Allewelt M, Lorenz J, et al. Moxifloxacin vs ampicillin/sulbactam in
aspiration pneumonia and primary lung abscess. Infection 2008; 36:23.
66. Bartlett JG. Anaerobic bacterial infection of the lung. Anaerobe 2012; 18:235.
67. Johanson WG, Pierce AK, Sanford JP. Changing pharyngeal bacterial flora of
hospitalized patients. Emergence of gram-negative bacilli. N Engl J Med 1969;
281:1137.
68. Smith Hammond C. Cough and aspiration of food and liquids due to oral
pharyngeal Dysphagia. Lung 2008; 186 Suppl 1:S35.
69. Ryu AJ, Navin PJ, Hu X, et al. Clinico-radiologic Features of Lung Disease Associated
With Aspiration Identified on Lung Biopsy. Chest 2019; 156:1160.
70. El-Solh AA, Vora H, Knight PR 3rd, Porhomayon J. Diagnostic use of serum
procalcitonin levels in pulmonary aspiration syndromes. Crit Care Med 2011;
39:1251.
71. Miyashita N, Kawai Y, Tanaka T, et al. Detection failure rate of chest radiography
for the identification of nursing and healthcare-associated pneumonia. J Infect
Chemother 2015; 21:492.
72. Claessens YE, Debray MP, Tubach F, et al. Early Chest Computed Tomography Scan
to Assist Diagnosis and Guide Treatment Decision for Suspected Community-
acquired Pneumonia. Am J Respir Crit Care Med 2015; 192:974.
73. Prendki V, Scheffler M, Huttner B, et al. Low-dose computed tomography for the
diagnosis of pneumonia in elderly patients: a prospective, interventional cohort
study. Eur Respir J 2018; 51.
74. Metlay JP, Waterer GW, Long AC, et al. Diagnosis and Treatment of Adults with
Community-acquired Pneumonia. An Official Clinical Practice Guideline of the
American Thoracic Society and Infectious Diseases Society of America. Am J Respir
Crit Care Med 2019; 200:e45.
75. Asai N, Suematsu H, Ohashi W, et al. Ceftriaxone versus tazobactam/piperacillin
and carbapenems in the treatment of aspiration pneumonia: A propensity score
 matching analysis. J Infect Chemother 2021; 27:1465.
76. Hasegawa S, Shiraishi A, Yaegashi M, et al. Ceftriaxone versus
ampicillin/sulbactam for the treatment of aspiration-associated pneumonia in
adults. J Comp Eff Res 2019; 8:1275.
77. Kadowaki M, Demura Y, Mizuno S, et al. Reappraisal of clindamycin IV
monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly
patients. Chest 2005; 127:1276.
78. Snydman DR, Jacobus NV, McDermott LA, et al. Lessons learned from the
anaerobe survey: historical perspective and review of the most recent data (2005-
2007). Clin Infect Dis 2010; 50 Suppl 1:S26.
79. Eykyn SJ. The therapeutic use of metronidazole in anaerobic infection: six years'
experience in a London hospital. Surgery 1983; 93:209.
80. Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic
infections. Am Rev Respir Dis 1979; 120:337.
81. Perlino CA. Metronidazole vs clindamycin treatment of anerobic pulmonary
infection. Failure of metronidazole therapy. Arch Intern Med 1981; 141:1424.
82. Germaud P, Poirier J, Jacqueme P, et al. [Monotherapy using amoxicillin/clavulanic
acid as treatment of first choice in community-acquired lung abscess. Apropos of
57 cases]. Rev Pneumol Clin 1993; 49:137.
83. Levison ME, Mangura CT, Lorber B, et al. Clindamycin compared with penicillin for
the treatment of anaerobic lung abscess. Ann Intern Med 1983; 98:466.
84. Gudiol F, Manresa F, Pallares R, et al. Clindamycin vs penicillin for anaerobic lung
infections. High rate of penicillin failures associated with penicillin-resistant
Bacteroides melaninogenicus. Arch Intern Med 1990; 150:2525.
85. Bai AD, Srivastava S, Digby GC, et al. Anaerobic Antibiotic Coverage in Aspiration
Pneumonia and the Associated Benefits and Harms: A Retrospective Cohort Study.
Chest 2024; 166:39.
86. Sladen A, Zanca P, Hadnott WH. Aspiration pneumonitis--the sequelae. Chest 1971;
59:448.
 87. Steiner J, Bachofen M, Bachofen H. Recovery from aspiration pneumonitis.
Pneumonologie 1974; 151:127.
88. Gipson SL, Stovall TG, Elkins TE, Crumrine RS. Pharmacologic reduction of the risk
of aspiration. South Med J 1986; 79:1356.
89. Lin L, Lv L, Wang Y, et al. The clinical features of foreign body aspiration into the
lower airway in geriatric patients. Clin Interv Aging 2014; 9:1613.
90. Abdulmajid OA, Ebeid AM, Motaweh MM, Kleibo IS. Aspirated foreign bodies in the
tracheobronchial tree: report of 250 cases. Thorax 1976; 31:635.
91. Brooks JW. Foreign bodies in the air and food passages. Ann Surg 1972; 175:720.
92. Kim IG, Brummitt WM, Humphry A, et al. Foreign body in the airway: a review of
202 cases. Laryngoscope 1973; 83:347.
93. Baharloo F, Veyckemans F, Francis C, et al. Tracheobronchial foreign bodies:
presentation and management in children and adults. Chest 1999; 115:1357.
94. HAUGEN RK. THE CAF'E CORONARY. SUDDEN DEATHS IN RESTAURANTS. JAMA
1963; 186:142.
95. Zavala DC, Rhodes ML. Foreign body removal: a new role for the fiberoptic
bronchoscope. Ann Otol Rhinol Laryngol 1975; 84:650.
96. LANSING AM, JAMIESON WG. Mechanisms of fever in pulmonary atelectasis. Arch
Surg 1963; 87:168.
97. Hedblom CA. FOREIGN BODIES OF DENTAL ORIGIN IN A BRONCHUS PULMONARY
COMPLICATION. Ann Surg 1920; 71:568.
98. Marchiori E, Zanetti G, Mano CM, Hochhegger B. Exogenous lipoid pneumonia.
Clinical and radiological manifestations. Respir Med 2011; 105:659.
99. Hadda V, Khilnani GC. Lipoid pneumonia: an overview. Expert Rev Respir Med
2010; 4:799.
100. Osman GA, Ricci A, Terzo F, et al. Exogenous lipoid pneumonia induced by nasal
decongestant. Clin Respir J 2018; 12:524.
101. Doubková M, Doubek M, Moulis M, Skřičková J. Exogenous lipoid pneumonia
caused by chronic improper use of baby body oil in adult patient. Rev Port
 Pneumol 2013; 19:233.
102. Spickard A 3rd, Hirschmann JV. Exogenous lipoid pneumonia. Arch Intern Med
1994; 154:686.
103. Kilaru H, Prasad S, Radha S, et al. Nasal application of petrolatum ointment - A
silent cause of exogenous lipoid pneumonia: Successfully treated with
prednisolone. Respir Med Case Rep 2017; 22:98.
104. Betancourt SL, Martinez-Jimenez S, Rossi SE, et al. Lipoid pneumonia: spectrum of
clinical and radiologic manifestations. AJR Am J Roentgenol 2010; 194:103.
105. Marchiori E, Zanetti G, Mano CM, et al. Lipoid pneumonia in 53 patients after
aspiration of mineral oil: comparison of high-resolution computed tomography
findings in adults and children. J Comput Assist Tomogr 2010; 34:9.
106. Gondouin A, Manzoni P, Ranfaing E, et al. Exogenous lipid pneumonia: a
retrospective multicentre study of 44 cases in France. Eur Respir J 1996; 9:1463.
107. Laurent F, Philippe JC, Vergier B, et al. Exogenous lipoid pneumonia: HRCT, MR,
and pathologic findings. Eur Radiol 1999; 9:1190.
108. Sung S, Tazelaar HD, Crapanzano JP, et al. Adult exogenous lipoid pneumonia: A
rare and underrecognized entity in cytology - A case series. Cytojournal 2018;
15:17.
109. Russo R, Chiumello D, Cassani G, et al. Case of exogenous lipoid pneumonia:
steroid therapy and lung lavage with an emulsifier. Anesthesiology 2006; 104:197.
110. Chin NK, Hui KP, Sinniah R, Chan TB. Idiopathic lipoid pneumonia in an adult
treated with prednisolone. Chest 1994; 105:956.
111. Lau C, Abdelmalak BB, Farver CF, Culver DA. Whole lung lavage for lipoid
pneumonia. Thorax 2016; 71:1066.
112. Abdelmalak BB, Khanna AK, Culver DA, Popovich MJ. Therapeutic Whole-Lung
Lavage for Pulmonary Alveolar Proteinosis: A Procedural Update. J Bronchology
Interv Pulmonol 2015; 22:251.
113. Chang HY, Chen CW, Chen CY, et al. Successful treatment of diffuse lipoid
pneumonitis with whole lung lavage. Thorax 1993; 48:947.
114. Orozco-Levi M, Torres A, Ferrer M, et al. Semirecumbent position protects from
pulmonary aspiration but not completely from gastroesophageal reflux in
mechanically ventilated patients. Am J Respir Crit Care Med 1995; 152:1387.
115. Loeb MB, Becker M, Eady A, Walker-Dilks C. Interventions to prevent aspiration
pneumonia in older adults: a systematic review. J Am Geriatr Soc 2003; 51:1018.
116. Fox KA, Mularski RA, Sarfati MR, et al. Aspiration pneumonia following surgically
placed feeding tubes. Am J Surg 1995; 170:564.
117. Spain DA, DeWeese RC, Reynolds MA, Richardson JD. Transpyloric passage of
feeding tubes in patients with head injuries does not decrease complications. J
Trauma 1995; 39:1100.
118. Alkhawaja S, Martin C, Butler RJ, Gwadry-Sridhar F. Post-pyloric versus gastric tube
feeding for preventing pneumonia and improving nutritional outcomes in
critically ill adults. Cochrane Database Syst Rev 2015; :CD008875.
119. Vilardell N, Rofes L, Arreola V, et al. A Comparative Study Between Modified Starch
and Xanthan Gum Thickeners in Post-Stroke Oropharyngeal Dysphagia.
Dysphagia 2016; 31:169.
120. Newman R, Vilardell N, Clavé P, Speyer R. Effect of Bolus Viscosity on the Safety
and Efficacy of Swallowing and the Kinematics of the Swallow Response in
Patients with Oropharyngeal Dysphagia: White Paper by the European Society for
Swallowing Disorders (ESSD). Dysphagia 2016; 31:232.
121. Logemann JA, Gensler G, Robbins J, et al. A randomized study of three
interventions for aspiration of thin liquids in patients with dementia or Parkinson's
disease. J Speech Lang Hear Res 2008; 51:173.
122. Robbins J, Gensler G, Hind J, et al. Comparison of 2 interventions for liquid
aspiration on pneumonia incidence: a randomized trial. Ann Intern Med 2008;
148:509.
123. Warusevitane A, Karunatilake D, Sim J, et al. Safety and effect of metoclopramide
to prevent pneumonia in patients with stroke fed via nasogastric tubes trial.
Stroke 2015; 46:454.
124. Allami A, Kianimajd S, Mavandadi S, Paybast S. Evaluation of domperidone efficacy
to prevent aspiration pneumonia in patients with acute ischemic stroke: a
randomized clinical trial. Acta Neurol Belg 2022; 122:1337.
125. Juthani-Mehta M, Van Ness PH, McGloin J, et al. A cluster-randomized controlled
trial of a multicomponent intervention protocol for pneumonia prevention among
nursing home elders. Clin Infect Dis 2015; 60:849.
126. Mody L. Editorial commentary: Preventing aspiration pneumonia in high-risk
nursing home residents: role of chlorhexidine-based oral care questioned again.
Clin Infect Dis 2015; 60:858.
127. Zimmerman S, Sloane PD, Ward K, et al. Effectiveness of a Mouth Care Program
Provided by Nursing Home Staff vs Standard Care on Reducing Pneumonia
Incidence: A Cluster Randomized Trial. JAMA Netw Open 2020; 3:e204321.
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