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Silent Aspiration: What Do We Know?
Deborah Ramsey, MA, MRCP,
1,2
David Smithard, BSc, MD, FRCP,
2
and Lalit Kalra, MD, PhD, FRCP
1
1
GuyÕs, KingÕs and St. ThomasÕSchool of Medicine, KingÕs College, London, and
2
Health Care of Older People Department, William Harvey
Hospital, Ashford, Kent, United Kingdom
Abstract. Although clinically evident aspiration is
common in subjects with dysphagia, a significant
proportion may aspirate silently, i.e., without any
outward signs of swallowing difficulty. This article
reviews the literature on the prevalence, etiology, and
prognostic significance of silent aspiration. An elec-
tronic database search was performed using silent
aspiration, aspiration, dysphagia, and stroke as
search terms, together with hand-searching of arti-
cles. Silent aspiration has been described in many
conditions and subgroups of patients (including
normal individuals), using a number of detection
methods, making comparisons a challenge. The best
data are for acute stroke, in which 2%–25%of pa-
tients may aspirate silently. Mechanisms associated
with silent aspiration may include central or local
weakness/incoordination of the pharyngeal muscu-
lature, reduced laryngopharyngeal sensation, im-
paired ability to produce a reflexive cough, and low
substance P or dopamine levels. In terms of prog-
nosis, silent aspiration has been associated with in-
creased morbidity and mortality in many but not all
studies. However, some degree of silent aspiration at
night may be normal in healthy individuals. The
phenomenon of silent aspiration is poorly understood
and further research is needed to improve methods of
detection and thereby better define its prevalence and
prognostic significance.
Key words: Dysphagia — Aspiration — Deglutition
disorders — Stroke.
Swallowing problems are common in a number of
disorders and may increase morbidity and mortality.
Patients with dysphagia are at increased risk of
aspiration, i.e., passage of food/fluid below the true
vocal cords into the airways, increasing the risk of
pneumonia and associated problems. In recent years
various studies have described aspiration which ap-
pears to be silent [1]: Material is inhaled without
coughing or other difficulties apparent at the bedside.
This article reviews the literature on silent aspiration,
including what is known of its prevalence, etiology,
and significance.
Search Strategy and Selection Criteria
Information was obtained from a literature search of
three electronic databases: Medline, Embase, and the
Cochrane Library, using silent aspiration, dysphagia,
aspiration, and stroke as search terms. The search
was supplemented by extensive hand-searching of
references. Papers not in the English language were
included if an abstract was available in English and
gave sufficient detail of the study to make it appro-
priate for consideration of inclusion. No time limit
was placed on the search history.
Definitions/Descriptions of Silent Aspiration
The first description of silent aspiration probably
appeared in 1937 [2]. The author described intro-
ducing a radiopaque agent into the mouths or naso-
pharynges of sleeping or stuporose subjects and
finding it radiographically in the bronchial tree the
following day, the implication being that it was
aspirated silently during sleep. In 1951, Culver et al.
Correspondence to: D.J.C. Ramsey, MA, MRCP, Department of
Stroke Medicine, GKT Medical School, Bessemer Road, London,
SE5 9PJ, United Kingdom. E-mail: deborah.ramsey@kcl.ac.uk
Dysphagia 20:218–225 (2005)
DOI: 10.1007/s00455-005-0018-9
[3] introduced blue dye into the stomachs of patients
before anesthesia and described a group who did not
vomit perioperatively but in whom dye was visible
bronchoscopically below the vocal cords after
surgery, presumably secondary to silent aspiration
during the procedure. A few years later, Gardner [4]
added barium to the diet of surgical inpatients and
subsequently demonstrated radiographically or
bronchoscopically the presence of thoracic barium in
10/94 patients. Subsequent work suggested that this
had probably followed aspiration while feeding; sev-
eral patients were drowsy and unwell, and one was
noted to cough during drinking, but in at least one
case aspiration was not suspected clinically and
therefore might be considered silent.
In 1983, Linden and Siebens [5] studied a small
group of dysphagic patients clinically and with vid-
eofluoroscopy in an attempt to correlate clinical
observations with radiologically demonstrated pene-
tration/aspiration. They were the first workers to coin
the phrase ‘‘silent penetration’’ in describing patients
who had laryngeal penetration on videofluoroscopy
but did not have any clinical manifestations of aspi-
ration, such as cough. It is unclear from their article
whether this group included all patients in whom
material passed into the laryngeal vestibule (pene-
tration) regardless of whether it passed below the true
vocal cords, or whether it included only individuals in
whom material passed below the cords (aspiration as
it is now understood).
Since then many studies of dysphagic patients
have used videofluoroscopy (VF). This is regarded by
many as the ‘‘gold standard’’ method of swallow
assessment [6] despite problems with its reliability [7].
Aspiration has been demonstrated on VF which was
without accompanying cough or obvious distress;
these occurrences were defined as silent aspiration
[1,8–15]. Others have used endoscopic methods to
study swallowing [16], i.e., fiberoptic endoscopic
evaluation of swallowing (FEES). The technique has
been used to demonstrate both silent and overt
aspiration [17,18] and is thought to be at least as
sensitive as VF at detecting swallowing difficulties [7].
Scintigraphic techniques with radioactive tracer have
also been used to identify silent aspiration [19–23].
Radioactive tracer is either delivered to the naso-
pharynx during or just before sleep, or it is added to a
soluble paste attached to the teeth before sleeping.
The detection of tracer in the thoracic region the
following day has been used as an indicator of silent
aspiration of the tracer during sleep, but these studies
cannot determine unequivocally whether tracer was
refluxed from the stomach, as demonstrated in other
scintigraphic studies [24], or directly aspirated from
the pharynx. In addition, apparent aspiration during
sleep may involve different mechanisms compared
with silent aspiration occurring during active
swallowing, as demonstrated in other scintigraphic
studies [25].
A possible indirect method of detecting silent
aspiration is by measuring desaturation on pulse
oximetry during swallowing. Collins and Bakheit [13]
suggested that desaturation of greater than 2%from
baseline during swallowing is indicative of aspiration.
However, pulse oximetry may lack the sensitivity to
detect such small changes reliably because the man-
ufacturerÕs error rate for the equipment is 2%. Other
studies have suggested that marked desaturation may
correlate better with penetration, regardless of whe-
ther aspiration also occurs, rather than with aspira-
tion alone [26,27]. Lim et al. [26] found that
desaturation on drinking aliquots of water occurred
in a group of probable silent aspirators (patients who
passed a bedside screen but subsequently aspirated on
endoscopic testing), but pulse oximetry was not per-
formed during the bedside assessment itself, pre-
venting better assessment of the correlation between
oximetry data and clinical findings.
If defined as aspiration without cough or other
sign of distress, silent aspiration is reliant for its
detection upon the use of techniques other than a
bedside clinical assessment, which, by definition,
cannot detect it. Although a number of methods have
been used to assess swallowing and aspiration (silent
or otherwise) in diverse patient groups, VF and
FEES, at present, are regarded as the best methods
despite their known limitations [7]. Since aspiration
represents a problem in the mechanisms of airway
protection during the swallow, this article focuses on
problems related to the oropharyngeal phases of
swallowing rather than the esophageal phase.
Prevalence of Silent Aspiration
Most studies on silent aspiration in dysphagic pa-
tients depend upon VF for detection. Linden and
Siebens [5] described 9/11 patients with asymptomatic
laryngeal penetration, 4 of whom did not cough even
on bronchial penetration. However, 10/11 patients
had a wet-hoarse voice, which is now known to be
suggestive of an unsafe swallow. Splaingard et al. [8]
found that 20%of 107 dysphagic inpatients under-
going rehabilitation aspirated silently on VF. Retro-
spective studies on large numbers (n‡1000) of
dysphagic patients who had undergone VF for vari-
ous reasons showed that 25%–30%aspirated silently
[9,10]. Leder et al. [17] studied swallow endoscopi-
D. Ramsey et al.: Silent aspiration: What Is Known? 219
cally and found that 28%of 400 dysphagic inpatients
aspirated silently.
Scintigraphic studies on small numbers of
sleeping patients have shown that 70%(7/10) of pa-
tients with a depressed conscious level developed
thoracic tracer [19] and 71%(10/14) of patients with
acute community-acquired pneumonia developed
positive scans [21]. Four studies [19–21,23] have de-
scribed signs of tracer in healthy individuals during
sleep using scintigraphic techniques which varied
considerably. Results ranged from the presence of
thoracic tracer in all 12 control subjects in one study
[23], to 45%(9/20) to 50%(5/10) of subjects in other
studies [19,20], and were as low as 10%(1/10) in one
study [21].
In contrast to these studies of sleeping healthy
subjects, a scintigraphic study [25] of swallowing in
awake dysphagic patients found positive results in 5/
14 (36%) patients and indeterminate results (residual
isotope in the neck region but not localizable specif-
ically to the esophagus or the airway) in 7/14 patients.
None of those with a positive scan had an absent
cough, although it was delayed in one; the exact
timing relative to the swallow was not documented so
it is hard to know whether this could represent silent
aspiration.
Silent Aspiration in Stroke
Dysphagia and aspiration have been studied most
frequently in stroke patients using VF, and silent
aspiration has been described as an occurrence sep-
arate from overt aspiration. Horner et al. [1,11] per-
formed two small studies of clinical predictors of
aspiration in dysphagic stroke patients (mean 2–3
months after stroke) that showed that 28%–38%pa-
tients aspirated silently. Holas et al. [12] studied
medical complications in dysphagic stroke patients
undergoing rehabilitation and found that 39%aspi-
rated silently.
Collins and Bakheit [13] compared pulse
oximetry with VF in the detection of aspiration in
dysphagic stroke patients and found that 15%of their
patients aspirated silently on VF. A scintigraphic
study in sleeping patients with acute pneumonia
showed that positive scans correlated with a history
of previous strokes [22]. Thoracic tracer was found in
more than 90%and more than 60%of patients with
previous bilateral and unilateral basal ganglia in-
farcts, respectively, but in less than 20%of patients
who had no history of cerebral infarcts.
These studies are summarized in Table 1, to-
gether with data from two of the larger studies of
dysphagic patients in which data for stroke patients
specifically are available [9,17]. The studies give
prevalence estimates for silent aspiration in subacute
dysphagic stroke patients of 15–39%, with significant
proportions of aspirators aspirating silently. How-
ever, the time between stroke and testing was very
variable and not always given. Other researchers [28–
32] (Table 1) specifically investigated unselected acute
stroke patients, often looking at the incidence and
predictors of aspiration or comparing methods of
swallow assessment. These workers described aspi-
ration in 21%–42%of acute stroke patients, with 2%–
25%aspirating silently. The studies were not designed
to assess prevalence, and numbers of silent aspirators
were generally small.
Silent Aspiration in Nonstroke Disease
Videofluoroscopy has been found to demonstrate si-
lent aspiration in many disorders incidentally; e.g.,
78%of subjects aspirated silently in a study of indi-
viduals with severe motor and intellectual disabilities
[33]. Arvedson et al. [14] retrospectively reviewed VF
results for 186 children with developmental dyspha-
gia and found that 26%had aspirated (94%silently).
Silent aspiration occurred on VF in 2/11 (18%) chil-
dren with chronic gastroesophageal reflux [34] and
has also been described in neurologically normal in-
fants without reflux [35].
Traumatic brain injury can cause dysphagia
and silent aspiration [36,37], and the prolonged
endotracheal intubation/ventilation often required in
such patients may contribute [38]. Tracheostomy
tubes have also been associated with aspiration, both
overt and silent; Elpern et al. [15], for example, found
50%of medically stable ventilated patients with tra-
cheotomies aspirated on VF and 77%of aspirations
were silent. Another study [18] tested swallowing
endoscopically and found that 33%of patients with a
recent (last two months) tracheotomy aspirated, 82%
silently. However, the causal link between tracheot-
omy and aspiration remains to be established [39].
Silent aspiration has been documented fol-
lowing cardiothoracic surgery [40], probably sec-
ondary to perioperative cerebrovascular events. Risk
factors for silent aspiration included older age, pre-
vious cerebrovascular disease, insulin-dependent
diabetes mellitus, previous myocardial infarction, and
chronic obstructive pulmonary disease. Silent aspi-
ration has also been demonstrated after treatment for
head/neck malignancies, with 22%of 49 previously
treated patients aspirating silently on VF in one study
[41]
.
Other conditions associated with silent aspira-
tion include ataxia–telangiectasia [42], myasthenia
gravis [43], ParkinsonÕs disease [44], and Down
220 D. Ramsey et al.: Silent aspiration: What Is Known?
syndrome [45]. It has been described secondary to
unilateral recurrent laryngeal nerve paralysis [46],
after pulmonary transplantation [47], after abdomi-
nal surgery [48], and possibly after oral contrast
administration for CT scanning [49]. Many of these
studies describe very small numbers of silent aspira-
tors, and again none of the work was designed to
study prevalence.
Etiology of Silent Aspiration
Silent aspiration may result from weakness/incoor-
dination of pharyngeal musculature [10], leading to
abnormal pharyngeal initiation of swallowing or
motor response. Similar difficulties may underlie the
association between prolonged endotracheal intu-
bation and silent aspiration: Intubation may impair
vocal fold motion [50], and tracheotomies may af-
fect the laryngopharyngeal movements of swallow-
ing and airway protection [15,51]. Central
neurological damage also seems important. In one
study dysphasia and more recent cerebrovascular
events were more common in silent than in overt
aspirators [8]. A scintigraphic study of elderly pa-
tients with pneumonia [22] also found more positive
scans and longer swallow latency responses in pa-
tients with previous basal ganglia infarcts than in
those without.
Another possible factor predisposing to silent
aspiration is reduced pharyngeal sensation [2], e.g.,
desensitization of the airways by prolonged intra-
tracheal intubation or tracheotomy [15]. Aviv et al.
[52] found that 11/18 stroke patients with no clinical
dysphagia had laryngopharyngeal sensory deficits
when tested with air pulses directed at mucosa
innervated by the superior laryngeal nerve. Although
the reaction to food/fluid may differ from that to air
pulses, pneumonia often developed in patients with
greater sensory deficits. Reduced local sensitivity has
also been demonstrated with increasing age [53],
perhaps contributing to the higher prevalence of
dysphagia in older patients; many studies have shown
an association between silent aspiration and in-
creased age [8,10,40].
Since ‘‘silent aspiration’’ describes aspiration
without coughing or other obvious distress, etiologic
theories must consider the integrity of the cough reflex,
which may be affected by impaired local/central neu-
romuscular control of diaphragmatic or chest wall
function [2,54]. There are actually two distinct types of
reflexive, nonvoluntary cough with different underly-
ing neurological mechanisms: a primary cough reflex
occurring at the level of the vocal folds, often referred
Table 1. Prevalence of silent aspiration in stroke
Researchers
Total patient
numbers in study Characteristics of patient group
%of patients
who aspirated
%of patients who
aspirated silently
%of aspirators
who aspirated silently
Garon et al. 1996 [9] 516
a
Dysphagic stroke patients (timing unknown) 60 16 42
Leder et al. 1998 [I7] 87
a
Dysphagic stroke patients (timing unknown) 47 20 41
Horner and Massey 1988 [1] 21 Dysphagic stroke patients, mean 2.8 months post stroke 52 38 73
Horner et al. 1988 [11] 47 Dysphagic stroke patients, mean 2.9 months post stroke 51 28 54
Holas et al. 1994 [12] 114 Dysphagic stroke patients, median 4 weeks from event 54 39 72
Collins and Bakheit 1997 [13] 54 Dysphagic stroke patients (timing unknown) 41 15 36
Nakagawa et al. 1997 [22] 45
b
Previous stroke
15 bilateral bg >90
15 unilateral bg >60
15 nil previous <20
Kidd et al. 1993 [30] 60 Acute strokes (within 72 hours) 42 8 20
Daniels et al. 1998 [29] 55 Acute strokes (within 5 days) 38 25 67
Smithard et al. 1998 [28] 94
b
Acute strokes (within 3 days) 21 11 50
Mann et al. 2000 [31] 128 Acute strokes (within 7 days) 22 2 7
Stanners et al. 1993 [32] 41
c
Acute strokes (within 2 days) 24 15 60
a
Data included only for stroke patients.
b
bg = basal ganglia infarcts. Exact numbers of aspirating patients not provided in paper.
c
Data given only for patients who underwent VF.
D. Ramsey et al.: Silent aspiration: What Is Known? 221
to as the laryngeal cough reflex, and a deeper tra-
cheobronchial cough reflex which tends to be delayed
and less productive. Although most workers studying
‘‘the cough reflex’’ do not differentiate between these,
often both are tested by the same procedure (e.g., in
looking for a cough response on swallowing), and it
seems likely that either or both reflexes may be affected
by stroke or similar neurological processes.
Many workers have demonstrated an associ-
ation between impaired cough and dysphagia/aspi-
ration in stroke [28,29,32,55–58]. Nakazawa et al. [59]
demonstrated depressed cough and delayed swallow
reflexes in patients with aspiration pneumonia. Niimi
et al. (60) found persistently higher cough thresholds
to inhaled irritants in patients with recurrent unex-
plained pneumonia than controls, suggesting that an
attenuated cough reflex may impair defenses against
the development of infections. Stephens et al. [61]
found an intact laryngeal cough reflex in 30 patients
with acute cerebral infarcts, irrespective of side of
infarct, despite an abnormal voluntary cough in 79%
of the 14 patients with a left-sided infarct. No pa-
tients developed aspiration pneumonia, and the
authors suggested that the laryngeal cough reflex is
more important for airway protection than the ability
to produce a voluntary cough. The occurrence of si-
lent aspiration during normal sleep, and especially in
association with a depressed conscious level [19], may
follow suppression during sleep of protective reflexes
involved in swallowing and airway protection, with
greater suppression in patients with impaired con-
sciousness.
Sputum levels of the neurotransmitter sub-
stance P are reduced in patients with aspiration
pneumonia [62], and recent scintigraphic work has
suggested that silent aspiration after stroke may
relate to low substance P levels. Arai et al. [63]
demonstrated an apparent reduction in silent aspi-
ration in hypertensive stroke patients, mediated via
increasing serum substance P concentrations [64],
following treatment with ACE (angiotensin-con-
verting enzyme) inhibitors; these potentiate sub-
stance P, which is otherwise degraded by ACE.
Upper respiratory tract epithelium contains nerve
plexuses using substance P, and the cough response
is attenuated by capsaicin, which abolishes sub-
stance P in the airway [64]. Angiotensin II receptor
antagonists seem less effective [65]. Dopaminergic
mechanisms also appear important, either directly
or by affecting substance P synthesis: levodopa
improves the swallowing reflex [66], and antipar-
kinsonian agents cabergoline and amantadine re-
duce silent aspiration in elderly patients after stroke
as efficiently as ACE inhibitors [67].
Prognostic Significance
It is possible that silent aspiration has outcomes
similar to overt aspiration [68]: gastric acid can cause
a chemical pneumonitis independent of bacterial
infection (MendelsonÕs syndrome), characterized by
acute respiratory distress and hypoxia. Alternatively,
aspirated particles may mechanically obstruct, caus-
ing acute or chronic respiratory distress and
increasing the risk of a secondary pneumonia.
Increased pulmonary complications and
poorer outcomes have been reported in surgical and
ventilated patients [40,69,70], but it is difficult to
disentangle the specific contribution of silent aspi-
ration. Pikus et al. [71] retrospectively reviewed pa-
tients who had undergone VF and found that those
with silent aspiration developed pneumonia more
often than those with normal swallowing, although
there was significant potential for selection bias in
their patient group determination. One study of
intubation injuries related silent aspiration to sub-
sequent pulmonary complications [50], and in the
group of normal infants found to have silent aspi-
ration [35], improvement of respiratory function
occurred only after resolution of dysphagia. Another
study in older, bed-bound, institutionalized patients
showed reduced pyrexial days (presumed respiratory
infections) by mouth-cleaning and maintenance of
an upright posture after meals [72] and concluded
that this had reduced silent aspiration of pharyngeal
secretions.
Within stroke patients there are conflicting
reports on the consequences of silent aspiration. One
review [73] found that pneumonia was infrequent in
dysphagic patients diagnosed at the bedside, sug-
gesting that silent aspiration (presumably undiag-
nosed clinically and therefore untreated) was
unimportant. In contrast, the scintigraphic study that
demonstrated silent aspiration in older patients after
stroke [22] found that pneumonia was more common
in patients developing positive scans, implying an
increased pneumonia risk from infarct-related silent
aspiration. Mortality was highest in patients who had
previously had bilateral cerebral infarcts. One study
[52] showed that 2/5 patients with bilateral laryngo-
pharyngeal sensory deficits developed aspiration
pneumonia compared with 0/13 patients with normal
sensation or unilateral deficits. Holas et al. [12] found
a fivefold increase in relative risk of pneumonia for
silently aspirating patients compared with overt/no-
naspirators, but they did not compare silent aspira-
tors with either group separately.
In contrast to studies that showed increased
risk of pulmonary complications and poor outcome,
222 D. Ramsey et al.: Silent aspiration: What Is Known?
Garcia et al. [48] described apparent silent aspiration
after extubation in a patient undergoing gastric sur-
gery several days after esophagogastroduodeno-
graphy with barium, with no clinical repercussions.
Garon et al. [9] have commented that individuals with
cerebral palsy and severe lifelong aspiration appear
only rarely to develop pneumonia. More objectively,
work by Langmore et al. [74] on independent pre-
dictors of aspiration pneumonia suggests that
dysphagia and aspiration (presumably including si-
lent aspiration) are necessary but not sufficient con-
ditions for the development of pneumonia. This is
supported by the observation that the occurrence of
silent aspiration in at least some healthy subjects
during sleep appears to have few common clinical
sequelae, suggesting either that it has minimal prog-
nostic significance in itself, or that healthy individuals
are better able to combat the organism load aspi-
rated, physically and immunologically, or that the
silent aspiration apparently detected by scintigraphic
studies during sleep is a different phenomenon from
(and not truly comparable with) silent aspiration that
occurs during swallowing in dysphagic individuals.
The lack of negative sequelae in healthy individuals
may simply reflect aspiration of secretions rather than
food textures.
Conclusions
The heterogeneity of patient groups, techniques, and
methodology of studies on silent aspiration has re-
sulted in considerable controversy on its prevalence,
etiology, and clinical consequences. It appears that
silent aspiration is a real phenomenon that probably
occurs in healthy individuals during sleep and in
many disease states. Although the exact prevalence
remains unknown because of the size and method-
ology of existing studies, the most reliable estimates
are for stroke, where it has been reported in 15%–
39%of subacute dysphagic stroke patients and in
2%–25%of acute unselected stroke patients. Mecha-
nisms that may underlie the occurrence of silent
aspiration include central or local weakness/incoor-
dination of the pharyngeal musculature, reduced
laryngopharyngeal sensation, impaired ability to
produce a reflexive cough, and low substance P or
dopamine levels. The consequences of silent aspira-
tion are unknown. Although some studies suggest
increased frequency of chest infections and poorer
clinical outcomes, other studies have shown no ad-
verse effects in mostly healthy individuals.
These controversies need to be addressed to
guide appropriate clinical management of patients at
risk of silent aspiration. Further studies looking at
silent aspiration should ideally develop methods of
detection more widely available than VF or FEES,
the techniques used most frequently to study it.
Defining true silent aspiration as aspiration that oc-
curs during swallowing, rather than during sleep,
would define a clinically relevant population group
for further study. Reliable methods of detection
would allow safe review of the appropriateness of
oral feeding after conditions such as stroke. The
uncertainty in management of silently aspirating pa-
tients can be resolved only if its etiology and conse-
quences are better understood.
Acknowledgment. The authors gratefully acknowledge support
from Action Medical Research and The Stroke Association.
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