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Aspiration pneumonia Pathophysiological
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PANMINERVA MED 2006;48:231-9
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Aspiration pneumonia
Pathophysiological aspects, prevention and management
A review
A. PETROIANNI, D. CECCARELLI, V. CONTI, C. TERZANO
Aspiration pneumonias occur more frequently than reported
and, in many cases, the disease is not recognised. In hospitalised
and institutionalised patients with predisposing diseases prompt
diagnosis of this complication and correct preventive measures
can drastically reduce the worsening of clinical conditions and
the deaths due to aspiration pneumonia. Normal airway structure, effective defence mechanisms, and preventive measures
are decisive in reducing aspiration episodes. An increased aspiration risk for food, fluids, medications, or secretions may lead
to the development of pneumonia. Pneumonia is the most common respiratory complication in all stroke deaths and in mechanical ventilation patients. In addition, the increased incidence of
aspiration pneumonia with aging may be a consequence of
impairment of swallowing and the cough reflex. Dysphagia,
compromised consciousness, invasive procedures, anaesthesia,
insufficient oral care, sleep disorders, and vomiting are all risk
factors. Aspiration pneumonia includes different characteristic
syndromes based on the amount (massive, acute, chronic) and
physical character of the aspirated material (acid, infected,
lipoid), needing a different therapeutic approach. Chronic
patients education and correct health care practices are the keys
for preventing the events of aspiration. In patients at risk a clinical and instrumental assessment of dysphagia should be evaluated. Management includes the removal of etiologic factors
(drugs, tubes, mobilisation, oral hygiene), supportive care, and
in bacterial pneumonias a specific antibiotic therapy for community-acquired or nosocomial events.
KEY WORDS: Pneumonia, aspiration - Dysphagia - Pneumonia,
prevention and control – Pneumonia, therapy.
A
spiration is defined as the inhalation of fluid
and secretions into the larynx and the lower res-
Received on February 16, 2006.
Accepted for publication on December 15, 2006
Address reprint requests to: Dr. A. Petroianni, Via Etruria 12, 00183
Roma, Italy. E-mail: angelo.petroianni@uniroma1.it
Vol. 48 - No. 4
Unit of Respiratory Diseases
Policlinico Umberto I
Fondazione E. Lorillard Spencer Cenci
University La Sapienza, Rome, Italy
piratory tract, and aspiration pneumonia is the pathologic consequence of this abnormal intake. Several
pulmonary syndromes may occur after aspiration,
depending on the amount and nature of the aspirated
material, its character (acid or neutral, infected or
sterile), the frequency of aspiration episodes, and the
host’s response.1 Some authors define as aspiration
pneumonitis (Mendelson’s syndrome) the chemical
injury caused by inhalation of sterile gastric contents, whereas aspiration pneumonia is the infectious
process caused by the inhalation of oropharyngeal
secretions that are colonized by pathogenic bacteria.2 In this review we define chemical inflammation
and infection as pneumonia, classifying the different syndromes in chemical, bacterial, and lipoid pneumonias.
Aspiration can be an acute or chronic process, and
it can occur in the community or in a hospital setting.
Even healthy subjects commonly aspirate, but normal
defence mechanisms usually clear the inoculum, and
these aspiration events rarely result in bacterial pneumonia.3 Aspiration pneumonia commonly occurs in
those individuals who tend to aspirate, because of dysphagia due to neurological disease or oesophageal disorders, central nervous system disorders, and altered
consciousness.4 Other risk factors for aspiration pneumonia include conditions in which the bacterial inoculum into the lung increases, such as periodontal disease,
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TABLE I.—Predisposing factors for pulmonary aspiration.
Compromised consciousness
— alcohol intoxication
— drug abuse
— anaesthesia
— neurological disorders
— psychiatric diseases
Dysphagia
— neurological disorders (Parkinson’s disease, stroke, myasthenia gravis, amyotrophic lateral sclerosis, multiple sclerosis)
— oesophageal disease (gastroesophageal reflux, achalasia, esophageal
cancer, structural abnormalities of the pharynx and oesophagus)
Invasive procedures of upper aerodigestive tract
— nasogastric and percutaneous feeding tubes
— endotracheal tubes
— tracheostomy
Vomiting
Periodontal diseases
Sleep disorders
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dental or tonsillar abscess, the ingestion of sedative
drugs, and any conditions that induce emesis.5
In addition, outside the hospital most cases are
observed in alcoholics, the elderly, those who spend
considerable time in the recumbent position, and the
generally debilitated.
The act of aspiration is usually not witnessed and the
clinical presentation is often very similar to other pneumonias: cough, chest pain, dyspnoea and fever.
However, symptoms tend to take days to weeks to
evolve and aspiration can lead to the development of
lobar or segmental pneumonia, weight loss, anaemia
and lung abscess or empyema.6
In this review we discuss pathophysiological mechanisms and clinical features as well as management and
preventive measures of aspiration pneumonia. An accurate anamnesis, direct or indirect, is essential to diagnose the disease and particularly to avoid relapses and
worsening of complex patients.
Epidemiology
Although pulmonary aspiration is an important cause
of serious illness and death, epidemiological data of
aspiration pneumonia are poorly defined: in some
papers7 its prevalence among all pneumonia was not
determined. Nevertheless, several studies indicated
that 5-15% of cases of community-acquired pneumonia are aspiration pneumonia.2
Aspiration pneumonia occurs most commonly in
hospitalised and institutionalised patients, particularly those with pre-existing predisposing factors such
as stroke, seizures and dysphagia due to several causes.1, 8 Aspiration pneumonia is the most common cause
of death in patients with dysphagia due to neurological disease, developing in approximately 500 000
patients per year in the US.9 Marrie et al.10 indicated
that the incidence of aspiration pneumonia in patients
with nursing home acquired pneumonia was 18% and
in control patients with community acquired pneumonia 5%.
Aspiration pneumonia occurs in 10% of patients
who are hospitalised after a drug overdose4, 11 and it is
the cause of 10-30% of all death with anaesthesia.12, 13
The incidence of aspiration pneumonia is likely to
rise, considering an increasing elderly population with
factors predisposing to aspiration.1, 14
232
Pathophysiology
The airway structure and the defence mechanisms
are decisive in reducing aspiration episodes. An effective cough mechanism, mucociliary transport system,
and normal function of the laryngeal tract allow good
protection for this complication.15 Founded on a structural airway analysis, some papers reported a more
frequent incidence for the right lung than the left. In fact
anatomically the right main bronchus shows a vertical
positioning more than the left main bronchus, and this
could promote aspiration episodes preferentially in
the right lung. Some pathological conditions, acute or
chronic, can predispose for aspiration pneumonia
(Table I). The predisposing factors for pulmonary aspiration are different in infants, in whom congenital airway defects or acute events prevail.5
There is a strong association between dysphagia
and the development of aspiration pneumonia. This
predisposing factor is the most frequent aetiology in
chronic patients.9, 16 Swallowing is a complex and
coordinately neuromuscular activity involving rapid
coordination of structure in the oral cavity, pharynx, larynx and oesophagus. It is described as involving 3
anatomical and temporal phases: the oral, the pharyngeal and the oesophageal. The first is under voluntary control, whereas the second 2 stages are involuntary, being under reflexive control.
The purpose of the first stage is to move food or
liquid from the oral cavity to the anterior faucial arches, where reflexive swallowing is initiated; during the
second stage, food is transported towards the oesoph-
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to the onset of the swallowing action. The latent time
(seconds) of swallowing was 1.2±0.1 in control subjects, 5.2±0.6 in patients with dementia, and 12.5±3 in
patients with aspiration pneumonia. The cough threshold was determined using various concentrations of
citric acid. The threshold concentration for citric acid
was 2.6±4 mg/mL in control subjects, 37.1±16.7
mg/mL in patients with dementia, and > 360 mg/mL
in patients with aspiration pneumonia.30 These results
showed that the increased incidence of pneumonia
with aging may be a consequence of impairment of
swallowing and the cough reflex with senescence.
Numerous studies have confirmed the effects of
ageing on swallowing.28, 29 The major finding of these
studies is that older people swallow more slowly, but
the safety of oropharyngeal swallowing is not compromised. However, the incidence of cerebrovascular
and degenerative neurological disease increases with
aging and these disorders are closely associated with
impaired swallowing and cough reflex and an increased
risk of aspiration.31
A clinical assessment of dysphagia should observe
parameters like oral control, lingual activity, oral
residue, laryngeal excursion, voice quality and coughing after swallowing. Available evidence, although
limited, suggests that a clinical assessment has approximately 80% sensitivity and 70% specificity for detecting aspiration in elderly adults.30 The instrumental
assessment supplements the clinical assessment. The
videofluoroscopic swallowing assessment (VFSS) is
the most utilized instrumental tool for determining
the nature and extent of swallowing disorders.32 It
identifies the disorders in movement patterns of the
oropharyngeal, laryngeal and oesophageal structures,
that may result in aspiration or inefficient swallowing. Limitations are imposed by patient cooperation,
timing of studies, and the ability to generalize to clinical settings.
In addition fiberoptic endoscopic evaluation of swallowing (FEES) can give information on anatomy, the
swallowing process, pharyngeal motility, and sensory
deficits.33, 34 Although aspiration cannot be observed
directly, it can be inferred from the residue left after
swallowing or ejection of material out of the trachea
after coughing. On comparison with VFSS in a small
sample of dysphagic patients, FEES gave better sensitivity values.32 This assessment can also be conducted at the bedside, and it is safe and well tolerated.
In recent years other clinically applicable methods
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agus; there is the velopharyngeal closure to prevent
the entry of food or liquid into the nasal cavity and
airway aspiration is prevented through elevation and
closure of the larynx. At the same time the cricopharyngeal region is open to allow bolus passage into the
oesophagus. The upper oesophageal sphincter (UES)
made up of cricopharyngeus attaches to the cricoid
cartilage. At rest, the UES closes to prevent reflux
from the oesophagus to the pharynx.17
One of the mechanisms that prevent aspiration during swallowing, such as vocal cord closure, aryepiglottic approximation, and laryngeal elevation, or during
gastroesophageal reflux, such as contraction of the
UES, may become impaired and this can lead to inhalation of food and to pneumonia.
Swallowing abnormality are a common functional
impairment of acute stroke, affecting as many as half
of all patients,18 and its detection is an important part
of acute stroke management.19 The literature suggests
that swallowing difficulties can affect 22-65% of stroke
patients, depending on the methods of assessment
used,20, 21 and may persist in some patients for many
months.22, 23 It is estimated that up to 38% of stroke victims die within the first month after stroke onset.
Pneumonia contributes to 34% of all stroke deaths
and represents the third cause of mortality in the first
month after stroke.24 After a stroke or other neurological event, the laryngeal cough reflex may be weakened
or absent. This increases the aspiration risk for food,
medications, fluids, or secretions past the true vocal
cords and may lead to the development of pneumonia.25
Loeb et al.26 investigated the risk factors for pneumonia in elderly residents of long-term care facilities.
In this study multivariated analysis revealed that difficulty swallowing food and medication were the most
important risk factors leading to pneumonia. Vergis
et al.27 identified witnessed aspiration and sedative
medications, which impair the cough reflex and swallowing, as the most important risk factors for pneumonia in a long-term facility.
An assessment of swallowing reflex, cough reflex,
and mucociliary transport system may determine the
critical level of depression in the defence system that
leads to aspiration pneumonia. Several methods to
assess these mechanisms have been reported.28, 29 In
one of these the swallowing reflex was induced by a
bolus injection of 1 mL of distilled water into the pharynx. The swallowing action was evaluated by the latency of the response, which was timed from the injection
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The overall mortality rate associated with massive
aspiration of gastric acid is approximately 30% and is
greater than 50% in patients with initial shock, secondary infectious pneumonia, or adult respiratory distress syndrome (ARDS).36
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for the assessment of the risk of aspiration pneumonia
in the elderly have been reported: the swallowing
provocation test (SPT) and the simple SPT (S-SPT)
proved very useful in differentiating patients with or
without stroke who are predisposed to aspiration.35
Classification of aspiration pneumonia
Aspiration pneumonia includes different characteristic syndromes based on the nature of the inoculum
and the inflammatory reaction. The amount and physical character of the aspirated materials determines
the different management.
Chemical pneumonia
Aspiration of gastric contents during vomiting may
have significant consequences and may occur after
sedation, anaesthetization,13 drug intoxication,11 gastrointestinal stasis or obstruction,36 autonomic dysfunction and other disorders.37
Vomiting with massive aspiration of gastric contents is a frequent phenomenon and is probably one of
the most frequent causes of aspiration disease in healthy
subjects. Chronic aspiration of gastric contents may
result from primary disorders of the larynx or the
oesophagus, such as achalasia, oesophageal stricture,
scleroderma, oesophageal carcinoma, and gastroesophageal reflux. Several studies have demonstrated
that the severity of lung injury increases directly with
the volume of the aspirate and with decreasing pH.38
Aspiration of pure gastric acid (pH<2.5) causes an
intense parenchymal inflammatory reaction, which
results in extensive desquamation of the bronchial
epithelium, bronchiolitis, pulmonary oedema, and
haemorrhage, mediated by inflammatory cells and
cytokines, including TNF-a, IL-8, and reactive oxygen
products.39, 40
The content of the stomach is generally sterile,
because the low pH of the gastric acid prevents the
growth of micro-organisms. Bacterial infection may
occur as a complication of the lung injury 2-3 days
after aspiration, or when the pH of the gastric content
is higher because of the use of antiacid, proton-pump
inhibitors, or histamine H2-receptor antagonists.16, 41
Moreover, there may be a gastric colonization by gramnegative bacteria in patients who receive enteric feedings, or in patients with gastroparesis or small bowel
obstruction.42
234
Bacterial pneumonia
Upper airway secretions and colonizing microorganisms are frequent causes of bacterial community
acquired and nosocomial aspiration pneumonias. It is
widely believed that silent aspiration into the intrathoracic airways is a common occurrence in normal subjects, and approximately half of all healthy adults aspirate small amounts of oropharyngeal secretions during
sleep.43
Pneumonia is usually prevented by mechanical and
immunological defence mechanisms such as coughing,
mucociliary clearance, airway and alveolar phagocytes. All these mechanisms, together with the low
burden of virulent bacteria in normal pharyngeal secretions, allow a clearance of the infectious material without consequence. Therefore, aspiration pneumonia
may follow if the aspirated inoculum is large enough,
or if mechanical, humoral, or cellular defences are
impaired. Huxley et al.3 injected small boluses of a
solution of 111In chloride into the nose of 20 normal
subjects and in 10 patients with coma or stupor, during nocturnal sleep. The results were that in 9 of the 20
normal subjects some 111In was found in lung
parenchyma the day after. They also observed that
sound sleep was a risk factor for aspiration of upper airway secretion. Other studies44 investigated whether
oral care lowers the frequency of pneumonia in the
institutionalised elderly. During follow-up, pneumonia
was diagnosed in 19% of participants who didn’t
receive oral care and in 11% of those who did.
In aspiration pneumonias several pathogens can be
isolated in the same patient. The predominant anaerobes include fusobacterium, clostridium species, and
members of the bacteroides fragilis group. The major
aerobic pathogens are Staphylococcus aureus,
Klebsiella pneumoniae, and Pseudomonas aeruginosa.45
Lipoid pneumonia
This syndrome is described separately because of its
peculiarity in inflammatory response through a granulomatous reaction. Lipoid material glides down the
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in a patient at risk, the diagnosis is usually based on
findings of hypoxemia, pulmonary infiltrates, fever
and leukocytosis. Rales, productive cough, wheezing,
or cyanosis are present in the majority of patients.
Anamnesis should investigate gastrointestinal conditions (vomiting, gastroesophageal reflux, achalasia,
hiatal hernia), neurological disorders, psychiatric illness, medications, alcoholism, surgical operations,
endoscopic procedures, sleep disorders, and periodontal diseases. Clinically chemical pneumonitis can
represent the onset of respiratory distress, with cough,
wheezing, fever, and tachypnea.
Radiographic findings in acute gastric acid aspiration include bilateral perihilar, ill-defined, alveolar
consolidations, multifocal patchy infiltrates, and segmental or lobar consolidation, which is usually localized to one or both lung bases.36 In bacterial pneumonias radiographic findings vary among the various
species of bacteria. Aspiration of infected material
results in a localized or lobar consolidation. Over a
period of weeks after aspiration, cavitation, abscess,
and empyema may occur. A prolonged clinical course
or large aspirations may result in severe necrotizing
bronchopneumonia.51
High resolution computed tomography (HRCT)
showed a great capacity to establish the severity of
the disease, especially for lipoid pneumonia (Figure 1).
In this syndrome CT hypodense images are assessed
by density measurement (Hounsfield Units, HU) or
by visual comparison with subcutaneous adipose tissue or by the “angiogram sign” on parenchymal window setting. A negative density (between –150 and
–30 HU) is highly suggestive of the presence of intrapulmonary fat.52
Lung function tests may reveal a normal or a restrictive ventilatory syndrome or a mixed syndrome; therefore, these parameters prove of less diagnostic value.
The transfer factor for carbon monoxide was frequently
abnormal.
The appearance of bronchoalveolar lavage may be
highly suggestive and the results of quantitative cultures
of samples obtained with a protected specimen brush
are particularly helpful for etiologic diagnosis. At differential cell count, various cytological profiles have
been described: macrophage alveolitis, lymphocytic
alveolitis and neutrophilic alveolitis.53
Microscopic and histological examination with specific stains (gram, sudan black, sudan red), and spectrophotometry or chromatography can be fundamental. Often the granulomatous form of the inflammato-
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respiratory tract without stimulating cough and is not
removed effectively by the cilia.46 The aspiration of a
massive amount of liquid paraffin and petroleum may
lead to an acute and fatal form of exogenous lipoid
pneumonia. The prognosis of this entity is usually
good if the disorder is quickly identified and the offending agent removed, unless the pneumonia is so widespread and severe, causing respiratory failure, or is
associated with a superimposed infection. Lipoid pneumonia may be complicated by hypercalcaemia due to
lipid granulomas, mycobacterial infection, progressive fibrosis or lung cancer.47 It is usually related to
accidental poisoning in children, but it is also observed
in fire-eaters.
Repeated inhalation of mineral oil or a related substance into the distal lung can lead to chronic lipoid
pneumonia. In adults it is related to the treatment of
constipation with paraffin oil48 and the repeated use of
oily nose drops for chronic rhinitis, mainly at bedtime. Animal fat, which can be hydrolysed to fatty
acids, causes more inflammation than vegetable or
mineral oils, but all types stimulate a chronic granulomatous inflammation, which tends to be located in
the lower or middle lobes. A clinical diagnosis may be
supported by bronchoalveolar lavage, transbronchial
biopsy, and specific stains (sudan black, sudan red,
oil red O).49
Diagnosis
In patients with aspiration pneumonia the aspiration episode is generally not seen.2 In some cases,
patients have no symptoms and the disease is an incidental finding. The diagnosis is, therefore, inferred
when a patient at risk for aspiration has radiographic
evidence of an infiltrate in a characteristic bronchopulmonary segment. Body position at the time of
aspiration determines which lung zones are dependent. In patients who aspirate while in a recumbent
position, the most common sites of involvement are the
posterior segments of the upper lobes and the apical
segments of the lower lobes, whereas in patients who
aspirate in an upright or semirecumbent position, the
basal segment of the lower lobes is usually affected.50
The process is similar to a typical community
acquired pneumonia, but, if not treated, they have a
higher incidence of complications such as cavitation
and lung abscess.45
After an observed or suspected episode of aspiration
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Figure 1.—High resolution computed tomography (HRCT) aspiration pneumonia. Ground-glass and reticulonodular infiltrates, and thick-walled
cystic spaces in the right lung.
ry cell reaction suggests a foreign body disease, and the
frequency of fibrosis lesions explains the potential
severity of the disease.
Differential diagnosis has to consider a non-aspiration pneumonia, ARDS, pulmonary oedema, pulmonary haemorrhage, immunoallergic or neoplastic
diseases.54 The diagnosis of aspiration pneumonia is
difficult, because the disease and its complications
can mingle. Relevant complications are acute respiratory failure, shock, ARDS, lung abscess, empyema,
necrotizing pneumonia, fibrosis, and systemic spread
of infection.
Data about microbiological diagnosis of aspiration
bacterial pneumonia are disparate. Several studies
enrolled patients observed relatively late, when complications such as necroziting pneumonia, lung abscess
or empyema had already occurred, and in these patients
anaerobic organisms were found to be the predominant
pathogens, from 62% to 100%, isolated alone or with
aerobes.49, 51
Furthermore, in many cases, it is impossible to isolate the responsible pathogens. Mier et al.55 studied
the bacteriology of early aspiration pneumonia with the
use of protected brushing. Positive results were
obtained for only 9 of 42 patients (47%). The recovered
pathogens were S.pneumoniae (28.5%), other
Streptococcus spp. (21.4%), S. aureus (14.3%), and
gram-negative bacilli (35.7%). In another study the
236
cultures were positive in 60% of patients. The most
common aerobic organisms were S. pneumoniae
(23%), Staphylococcus spp. (29%), and gram-negative bacilli (40%).
However, significant isolation of anaerobic bacteria
in patients suffering from lower respiratory tract infection is difficult, because it requires specific sampling
techniques, adequate transport conditions and specific growth media.
Prevention and prognosis
Aspiration pneumonia in many cases is a preventable
disease requiring attention to patient care. A semirecumbent position, as opposed to supine, may prevent
aspiration pneumonia by minimising gastroesophageal
reflux and subsequent inhalation of gastric contents.56
Oral hygiene and dental prophylaxis may reduce the
oral pathogenic bacilli load in subjects who have a
high rate of aspiration and in elderly nursing home
patients.14, 57 In these patients an assessment of swallowing, with a videofluoroscopic swallowing study
and/or endoscopic evaluation, could also be necessary.
There are contradictory aspects to the issue of feeding tubes and aspiration pneumonia. Feeding tubes
have to be managed properly. The position of oral
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First of all the disease (gastroesophageal, neurological, psychiatric) or the process (medications, alcoholism, feeding tubes) inducing aspiration pneumonia
should be treated.
Many nosocomial aspiration events represent chemical pneumonia and do not require antibiotic therapy.
However, antibiotic therapy is commonly indicated
in patients with aspiration pneumonia, because many
patients are debilitated or immunocompromised, and
so at increased risk for infectious pneumonia. The
choice of the antibiotic should depend on the setting in
which the aspiration occurs as well as the patient’s
general health.
In the case of community-acquired aspiration pneumonia, empiric treatment must principally cover anaerobic and streptococcal species. The usual oropharingeal flora is most likely involved in communityacquired cases, and treatment with penicillin is generally sufficient.45 Recommended antibiotic regimens
include penicillin and beta-lactamase inhibitor combinations, such as ampicillin/sulbactam or amoxicillin/clavulanate, or clindamycin. Fluoroquinolones,
such as levofloxacin and moxifloxacin, have reasonable anaerobic activity and achieve high concentrations in endobronchial secretions and lung tissue.
Patients at risk for nosocomial pneumonia must be
treated for gram-negative enteric bacilli and staphylococci, until culture results are available to guide therapy.36 Nosocomial aspiration pneumonia often occurs
in very sick patients with modified oral flora, and
abnormalities of the gastrointestinal tract, that favour
the proliferation of gram-negative species.45 Possibly,
it is wise to base the treatment on the results of quantitative cultures of samples obtained with a protected
specimen brush.45 The risk of aggressive pathogens,
such as Pseudomonas aeruginosa and Acinetobacter
species, is highest in patients in intensive care units and
those in mechanical ventilation. Patients with coma,
diabetes mellitus, or end-stage renal disease are at
high risk for staphylococcal pneumonia. Therefore,
patients with nosocomial aspiration pneumonia may
receive cephalosporin, such as cefepime or ceftazidime,
and clindamycin or metronidazole. An effective alternative may be penicillin and beta-lactamase inhibitor
combination, such as ampicillin/sulbactam,60
piperacillin/tazobactam, or ticarcillin/clavulanate. For
patients allergic to penicillin, fluoroquinolones or a
clindamycin and aztreonam combination may be considered. Vancomycin should be used for antistaphy-
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feeding tubes should be monitored because they can
easily become displaced over time.58
On the other hand, it is reasonable to believe that
feeding tubes reduce the risk of aspiration pneumonia
in some patients with swallowing difficulties, but they
offer no protection from aspiration of oral secretions.
Correct education of patients at risk and the sensitisation of health care personnel are the keys for preventing this serious complication. Guidelines for preventing health-care- associated pneumonia have been
reported by the Center for Disease Control and
Prevention of US (CDC).59
Prognosis of aspiration pneumonia varies considerably in the different studies because of the several
confusing parameters involved in the mortality rate. In
numerous series most deaths appeared to be attributable to the aspiration rather than to the disease leading
to the aspiration.59 Nevertheless in Hickling’s study7
the mortality rate appears low (21%), and the deaths
have been most often attributable to underlying illness than to an aspiration event. Another study16 has
demonstrated a crude mortality of 22% and an attributable mortality linked to pneumonia of 11%, after
excluding patients who died as a result of diseases
leading to aspiration.
The severity of the aspiration event is relevant for the
mortality rate. Massive aspiration showed a mortality
rate of 70%, whereas aspiration pneumonia complicated by empyema showed a mortality of 20%. For
uncomplicated pneumonia the mortality rate was
approximately 5%.7
Management
All patients with aspiration pneumonia need supportive care as well as specific treatment. Oxygen supplementation and i.v. hydration may be necessary. The
upper airway should be suctioned if feeding tube, foreign material, or secretions are still present in the
oropharynx. Suctioning should be properly performed
to avoid inducing gagging and emesis.
Endotracheal intubation may be necessary in patients
unable to protect their airways, with altered mental status, or persistent hypoxia. Positive pressure mechanical
ventilatory support may be required in severe cases.
The therapeutic approach for aspiration pneumonia is based on the knowledge of the presumable etiologic factor, through accurate anamnesis, clinical and
instrumental data.
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6. Marom EM, McAdams HP, Erasmus JJ, Goodman PC. The many
faces of pulmonary aspiration. Am J Roentgenol 1999;172:121-8.
7. Hickling KG, Howard R. A retrospective survey of treatment and
mortality in aspiration pneumonia. Int Care Med 1988;14:617-22.
8. Teixeira A, Cherin P, Demoule A, Levy-Soussan M, Straus C, Verin
E et al. Diaphragmatic dysfunction in patients with idiopathic inflammatory myopathies. Neuromuscul Disord 2005;15:32-9.
9. Marik PE, Kaplan D. Aspiration pneumonia and dysphagia in the
elderly. Chest 2003;124:328-36.
10. Marrie TJ, Durant H, Kwan C. Nursing home-acquired pneumonia:
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11. Aldrich T, Morrison J, Cesario T. Aspiration after overdosage of sedative or hypnotic drugs. South Med J 1980;73:456-8.
12. Olsson GL, Hallen B, Hambraeus-Jonzon K. Aspiration during anaesthesia: a computer-aided study of 185,358 anaesthetics. Acta
Anaesthesiol Scand 1986;30:84-92.
13. Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology
1993;78:56-62.
14. Watando A, Ebihara S, Ebihara T, Okazaki T, Takahashi H, Asada M
et al. Daily oral care and cough reflex sensitivity in elderly nursing
home patients. Chest 2004;126:1066-70.
15. Teramoto S, Ishii T, Yamamoto H, Yamaguchi Y, Namba R, Hanaoka
Y et al. Significance of chronic cough as a defence mechanism or a
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lococcal coverage in hospitals with methicillin-resistant S. aureus. Treatment for 7-10 days appears adequate for patients who respond promptly. Therapy
should be extended from 14 to 21 days if highly resistant pathogens, such as P. aeruginosa or Acinetobacter
species, are isolated. Patients with lung abscess, cavitary pneumonia, or empyema require long-term treatment for 4-8 weeks or more.1
Corticosteroids have been used for decades in the
management of aspiration pneumonia, but there are
limited data to support this practice. Studies were generally unsuccessful and sometimes the outcomes were
worse for those treated with corticosteroids.
The patient’s clinical course should be monitored.
Prompt clinical response over the first few days, including rapid clearing of pulmonary infiltrates, could suggest chemical pneumonitis rather than bacterial pneumonia.
Conclusions
Pulmonary involvement and symptoms in hospitalised and institutionalised patients with compromised consciousness, dysphagia, invasive procedures,
vomiting, neurological or psychiatric disease, or treated with sedative drugs should make us suspicious of
aspiration pneumonia. Management of these patients
is complex because of severe concomitant diseases.
Antimicrobial therapy for aspiration pneumonia is
often empirical and should be based on patient characteristics. It is essential to know the setting in which
aspiration occurred, the severity of pneumonia, and
information regarding local pathogens and resistance
patterns, and, last but not least, an accurate anamnesis
for reducing the mortality rate and avoiding chronic and
irreversible compromise of lung parenchyma.
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