Chem. Senses 27: 617-622,
2002
© Oxford University Press 2002
Anti-inflammatory and Surgical Therapy of Olfactory Disorders Related to Sino-nasal Disease
1 Department of Otolaryngology, Head and Neck Surgery, University of Basel, Basel, Switzerland 2 Department of Otorhinolaryngology, University of Dresden Medical School, Dresden, Germany
Correspondence to be sent to: Markus Wolfensberger, Department of Otolaryngology, Head and Neck Surgery, University Hospital, CH-4126 Basel, Switzerland. e-mail: mwolfensberger{at}uhbs.ch
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Abstract |
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 Top Abstract IntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Olfactory loss may be caused by mechanical obstruction or inflammation of the olfactory epithelium due to allergic/non-allergic rhinitis and chronic sinusitis with or without polyps. Treatment of olfactory loss related to sino-nasal disease is possible. Apart from surgical approaches and/or treatment with antibiotics, both systemic and topical steroids are effectively used in the therapy of olfactory loss related to sino-nasal disease. In most cases improvement of olfactory function appears to relate to the anti-inflammatory actions of the steroids used. While some details of therapeutic effect and dose regimen are not clear, systemic steroids are often helpful even in patients without nasal obstruction due to polyps or obvious inflammatory changes.
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Introduction |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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A free nasal passage is the prerequisite of olfactory function. Olfactory loss is encountered when this passage is mechanically blocked or when the intranasal air flow is altered such that the transport of odor molecules to the olfactory epithelium is affected (Mott and Leopold, 1991
; Smith and
Duncan, 1992; Knecht et
al., 1999). In this context it is important to point out that
the olfactory epithelium is mainly localized in the olfactory cleft
(von Brunn, 1892;
Read, 1908;
Leopold et al., 2000)
with a typical width of 1-2 mm. The cleft is easily obstructed by mucosal
congestion or polypoid changes of the mucosa. The nasal airway, however, may
remain intact despite this congestion within the nasal vault.
In addition to mechanical obstruction, inflammation of the olfactory
epithelium also appears to affect olfactory function
(Jafek et al., 1987;
Klimek and Eggers, 1997;
Stevens, 2001). Finally,
olfactory magnitude also depends on the perceived effort associated with a
sniff, which is frequently increased in sino-nasal disease (SND)
(Teghtsoonian and Teghtsoonian,
1984; Youngentob et
al., 1986; Hornung et
al., 1997). For example, perceived odor strength is reduced
when subjects sniff against increasing resistances while the nasal flow rate
remains constant (Youngentob et
al., 1986). Consequently, olfactory loss is a characteristic
complication of SND which is related to both nasal obstruction and
inflammatory changes of the olfactory epithelium.
|
Causes of SND-related olfactory loss |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Olfactory loss following SND has different causes (Doty and Frye, 1989
;
Mott and Leopold, 1991). Among
them are inflammatory conditions (allergic and non-allergic rhinitis and
chronic sinusitis with or without polyps), neoplasms and scars following
surgery, (Duncan and Smith,
1995; Cullen and Leopold,
1999; Seiden and Duncan,
2001). In a study of 53 patients with SND-related olfactory loss
21 had chronic sinusitis with nasal polyps, 19 had chronic sinusitis without
polyps, eight had allergic rhinitis, two had post-surgical trauma, one had
atrophic rhinitis and one had an inverting papilloma [cited from Seiden
(Seiden, 1997)]. In patients
with allergic rhinitis it has been shown that the degree of olfactory loss is
correlated with the presence of eosinophilic cationic protein, which is known
to be a sensitive marker of allergies found in the mucus. This correlation
(r = 0.83) was significantly higher than the correlation between
olfactory loss and nasal obstruction assessed by means of rhinomanometry
(r = 0.65) (Klimek and Eggers,
1997). It is unclear, however, how inflammation can affect
olfactory function so dramatically in some patients that it leads to an almost
complete suppression of olfactory function
(Kern, 2000). |
Frequency of SND-related olfactory loss |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Olfactory loss is found in approximately one quarter of patients with chronic sinusitis without polyps but in up to 83% of patients with chronic sinusitis with polyps (Delank and Stoll, 1994
; Lund and Scadding,
1994; Bonfils et al.,
1998). In allergic rhinitis approximately 15% present with
olfactory loss (Cowart et al.,
1993) [compare Seiden et al.
(Seiden et al.,
1989)]. Considering that 10-15% of the general population suffer
from allergic rhinitis (Cowart et
al., 1993) and 
14% of the population report chronic
sinusitis (Lieu and Feinstein,
2000), an impressive number of people are compromised by
SND-related olfactory dysfunction. |
Subjective symptoms |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Common characteristics of SND-related olfactory loss include a gradual decrease in olfactory function over several years and fluctuations of olfactory function, e.g. temporary improvement through physical exercise or the spontaneous restoration of olfactory sensitivity for a few moments (Mott and Leopold, 1991
;
Smith and Duncan, 1992)
[compare Hill and Jafek (Hill and Jafek,
1989)]. Such fluctuations are seen in 45% of patients with
SND-related olfactory loss (Seiden,
1997). The presence of parosmia or phantosmia has also been
described in SND-related olfactory loss. This seems to be much more
characteristic of olfactory dysfunction following upper respiratory tract
infections (Nordin et al.,
1996; Hummel and Knecht,
2001; Seiden and Duncan,
2001). Some patients with SND-related olfactory loss may have no
other nasal symptoms, e.g. respiratory dysfunction. This is due to the fact
that, in healthy subjects, the largest portion of the respiratory airstream
primarily passes through the middle and some of the inferior meatus of the
nasal cavity; it is estimated that only 10-15% of the respiratory air reaches
the olfactory cleft (Masing,
1967; Scherer et al.,
1989).
It is interesting to note that many people with SND-related olfactory loss
are apparently not disturbed by this sensory impairment
(Hosemann et al.,
1993). Only one third of SND patients with confirmed olfactory
loss complain of decreased olfactory function. When specifically asked for the
presence of olfactory loss, half of SND patients report hyposmia; the other
half of SND patients are not aware of this olfactory loss, even when anosmia
is present (Doty and Frye,
1989; Delank and Stoll,
1994). This situation is comparable to age-related loss of
olfactory function where many elderly people are not aware of an impaired
sense of smell. In both scenarios olfactory function decreases gradually over
several years (Nordin et al.,
1995). Thus it appears that many people adjust to the slow onset
of olfactory loss. In addition, there are preliminary data indicating that
these adjustments also include changes in sensitivity in the gustatory and
trigeminal systems (Hummel,
2000; Hummel et al.,
2001). In contrast, adjusting to sudden olfactory loss seems to be
much more difficult, e.g. in olfactory loss following upper respiratory tract
infections (post-URTI) or head trauma
(Hendriks, 1988) where, in the
majority of cases, the olfactory loss is clearly recognized.
This may also influence estimates of the relative frequency of SND-related
olfactory loss (Douek, 1970;
Doty, 1979;
Henkin et al., 1981;
Fikentscher et al.,
1983; Davidson et al.,
1987; Hendriks,
1988; Deems et al.,
1991; Mott and Leopold,
1991; Temmel et al., 2001). Of all patients who present
themselves to specialized centers 10-77% suffer from an olfactory loss
due to SND, 3-33% from post-traumatic olfactory loss, 14-40% from post-URTI
olfactory loss and 1-30% from olfactory loss related to other causes (e.g.
congenital olfactory loss, olfactory loss through toxic substances,
drug-induced olfactory loss and olfactory loss through neurodegenerative
disease). In up to 26% of the cases impairment of the sense of smell is
diagnosed as idiopathic. When contemplating these figures it must be kept in
mind that most of these statistics are based on highly selected populations.
It can be assumed that many people with olfactory loss are first
counseled/treated by a general practioner, an otorhinolaryngologist or a
neurologist. As there are therapeutic opportunities in SND-related olfactory
loss, it can be assumed that many ORL specialists are able to effectively
counsel SND patients and that SND-related olfactory loss may be treated
effectively in many cases (see below). Consequently, the number of patients
with SND-related olfactory loss is probably grossly underestimated.
|
Objective symptoms |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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The dominant symptom of the putrid form of chronic sinusitis is mucosal discharge, particularly post-nasal drip. In contrast, the polypoid form of chronic sinusitis is dominated by decreased respiratory air flow. Both forms of chronic sinusitis are often accompanied by pain and/or sensations of pressure.
In SND patients the degree of olfactory loss is correlated with the degree
of nasal obstruction (Damm et al.,
2000). Interestingly, however, there is only a weak correlation
between duration of nasal obstruction and degree of olfactory loss
(Min et al., 1995;
Apter et al., 1999).
Olfactory loss is found in only 25-29% of patients with chronic sinusitis
without polyps, but in 76-83% of patients with chronic sinusitis with polyps
(Delank and Stoll, 1994;
Lund and Scadding, 1994;
Bonfils et al., 1998).
In addition, in patients with chronic sinusitis without polyps only 4% are
diagnosed as anosmic, whereas 31% of patients with polyps are anosmic
(Bonfils et al., 1998;
Delank and Stoll, 1998).
Patients with perennial rhinitis have been reported to exhibit decreased
olfactory thresholds, odor discrimination and odor identification throughout
the entire year; in contrast, when patients with seasonal allergic rhinitis
are tested during the symptom-free interval only thresholds have been found to
be altered (Klimek and Eggers,
1997; Moll et al.,
1998). More recent work indicates that the degree of olfactory
loss is related to the degree of the allergic condition. Specifically, it has
been suggested that olfactory loss is related to the number of items patients
are allergic to (Schickinger et
al., 2000).
Work-up of patients with SND should include a detailed endoscopic
examination of the nasal cavity. This is superior to anterior rhinoscopy,
which has a false negative rate of 50% in patients with SND-related
olfactory loss (Seiden, 1997).
In addition, a coronal CT scan should be performed even in cases where
endoscopy is unremarkable (Seiden and
Duncan, 2001). Other investigations may include bacteriological
and/or cytological analyses, allergy testing
(Simola and Malmberg, 1998),
measurements of nasal air flow using anterior rhinomanometry
(McCaffrey, 1991),
measurements of nasal volume, e.g. acoustic rhinometry, or, in highly
specialized centers, biopsies from the respiratory and/or olfactory epithelium
(Lovell et al., 1982;
Roithmann et al.,
1994; Hamilton et
al., 1995; Min and Jang,
1995).
|
Therapy of SND-related olfactory loss |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Therapy of typical SND-related olfactory loss follows a step-wise procedure. In cases of purulent chronic sinusitis antibiotics may be tried. Steroids, used either systemically or locally, are prescribed in patients with chronic sinusitis. Finally, when medical therapy fails, surgical tretament is indicated (Mott and Leopold, 1991
). Conservative therapy of SND-related olfactory loss
Antibiotics
Most frequently putrid acute siunusitis is governed by Streptococcus
pneumoniae, Haemophilus influenzae and Moraxella catarrhalis,
which are relativley sensitive to antibiotic therapy. However, in the chronic
form of putrid sinusitis Staphylococcus aureus and Pseudomonas
aeruginosa are much more important. Whenever possible antibiotic therapy
should only be started after the bacteria have been identified and tested for
resistance to antibiotics. It is important to note that in chronic putrid
sinusitis antibiotic treatment is not always succesful.
Steroids
Among many other effects corticosteroids act as anti-inflammatory drugs,
the effects of which are produced via a number of different pathways,
including inhibition of phospholipase A2 through induction of lipocortin
(Fong et al., 1999).
They reduce submucosal edema and mucosal hypersecretion and thereby increase
nasal patency. Although not yet proven in an appropriate double blind study,
steroids are of help in many SND patients
(Golding-Wood et al.,
1996; Mott et al.,
1997; Tos et al.,
1998; Seiden and Duncan,
2001). For example, most recently Stevens reported that systemic
administration of steroids was effective in 12 of 24 patients with SND-related
olfactory loss (Stevens,
2001). In addition to the anti-inflammatory activity it has been
postulated that corticosteroids directly improve olfactory function
(Mott and Leopold, 1991;
Klimek and Eggers, 1997) by
modulating the function of olfactory receptor neurons through effects on
olfactory Na,K-ATPase (Fong et
al., 1999). In fact, also based on our own experience,
systemic steroids are often helpful even in patients without nasal obstruction
due to polyps or obvious inflammatory changes (compare
Jafek et al., 1987;
Stevens, 2001).
Steroids may be administered systemically or topically. With regard to
olfactory dysfunction, systemic administration is often applied for diagnostic
purposes. If systemic steroids improve olfactory function, treatment is
continued with locally administered steroids. Although systemic steroids are
usually more effective than locally administered steroids
(Mott and Leopold, 1991;
Ikeda et al., 1995),
prescription of systemic steroids over an extended period of time is rarely
warranted (Hotchkiss, 1956;
Jafek et al., 1987).
Side effects such as diabetes, gastric ulceration, osteoporosis, hypertonia,
depression or sleeping disorders clearly limit the systemic use of steroids
for the treatment of olfactory disorder
(Scott, 1989). While exact
recommendations are missing, it is possible, however, to repeatedly administer
short courses of systemic steroids with an interval of 6-12 months between
courses. In fact, some of our patients regularly ask for a course of steroids
over christmas (which in Germany and Switzerland is a truly olfactory
period).
A number of studies indicate the usefulness of topical steroids
(Golding-Wood et al.,
1996; Mott et al.,
1997; Tos et al.,
1998), however, the role of topical steroids in the treatment of
SND-related olfactory loss has not been clearly established
(Mott and Leopold, 1991;
El Naggar et al.,
1995; Ikeda et al.,
1995). So far, no factors predicting a favorable response to
topical stroids have been identified. Finally, little information is available
on the efficacy of this treatment over an extended period of time.
Systemic steroids are more effective than locally administered steroids
(Mott and Leopold, 1991;
Ikeda et al., 1995).
For example, 30 of 36 patients experienced an improvement in their sense of
smell when put on systemic steroids, however, this was the case in only 13 of
52 patients following application of topical steroids
(Seiden and Duncan, 2001). For
locally administered steroids one double blind study has been performed in
patients with seasonal allergy using mometasone (n = 80) or placebo
(n = 41) (Meltzer et
al., 1998). Upon assessment with tests for odor
identification and n-butanol odor thresholds baseline levels before
treatment were found to be normal, which may have contributed to the lack of
significant differences between placebo and mometasone. It is not entirely
clear why systemic steroids have a higher therapeutic efficacy compared with
topical steroids (Ikeda et al.,
1995; Seiden and Duncan,
2001). One reason may relate to the deposition of the spray in the
nasal cavity. In fact, it has been shown that only a small volume of nasally
applied sprays reach the olfactory epithelium, which is situated in an
effectively protected area of the nasal cavity
(Hardy et al., 1985;
Newman et al., 1987;
McGarry and Swan, 1992).
Considering that the dominant function of the nose is heating, humidification
and filtering inspired air it becomes clear that little or nothing of applied
sprays reach the olfactory epithelium. This situation can be improved by the
application of sprays in a `head-down forward position'
(Mott and Leopold, 1991).
Other reasons for the greater efficacy of systemic steroids may relate to the
site of action of steroids in SND patients. It has been speculated that the
site of inflammation relevant to olfactory loss may not always be in the
mucosa but in the area of the cribriform plate or the olfactory bulb
(Wolf, 1998;
Roob et al., 1999).
This hypothesis appears particularly attractive in patients who respond to
systemic steroids, have no apparent signs of nasal inflammation and do not
respond to locally administered steroids.
In addition to the use of steroids there are still other therapeutic
approaches to restoration of olfactory loss. They include the use of
antileukotrienes (Parnes and Chuma,
2000), saline lavage (Bachmann
et al., 2000) or approaches which have received less
vigorous scientific investigation, e.g. diet changes
(Rundles, 1946), anti-allergy
immunotherapy (Stevenson et al.,
1996) and herbal treatments.
Surgical therapy
Surgical therapy aims at both elimination or reduction of nasal obstruction
and removal of inflamed mucosa or polyps
(Jafek and Hill, 1989). Today
this type of surgery is routinely performed endonasally under endoscopic or
microscopic control.
Most of the patients undergo surgery to remedy decreased nasal patency, a
feeling of pressure or recurrent infections of the nasal sinuses. Surgery is
rarely performed to specifically treat olfactory dysfunction. In spite of
this, post-operative improvement of olfactory function has been reported by
50-100% of patients (Lund and Scadding,
1994; Min et al.,
1995; Downey et al.,
1996; Delank and Stoll,
1998). Frequently, however, olfactory recovery is incomplete
(Lund and Scadding, 1994).
When olfactory function is measured, one study found an improvement in 25% of
patients with pre-operative hyposmia and 5% with pre-operative anosmia
(Delank and Stoll, 1998).
Following surgery, others (Min et
al., 1995) reported the percentage of normosmic patients
increased from 22 to 36%.
In addition, a study reported severe impairment of olfactory acuity in 24
patients prior to excision of the inferior turbinates
(Ophir et al., 1986).
Post-operative improvements of olfactory acuity were statistically
significant. None of the patients exhibited elevated thresholds compared with
pre-operative results; in two anosmic patients olfactory loss could not be
remedied.
Predictors of treatment outcome in terms of improvement of olfactory
function have not been identified. Neither the degree of pre-operative
obstruction nor the duration of olfactory loss correlate with therapeutic
success. Similarly, findings of post-operative endoscopical investigations do
not correlate with the improvement in the sense of smell
(Hosemann et al.,
1993). This is not altogether surprising, since polypoidal mucosa
is usually not removed from areas superior to the upper turbinate/olfactory
cleft underlying the cribriform plate.
While beneficial in most cases, surgery may also pose a certain risk to
olfactory function. Formation of synechiae (mucosal adhesions), crusting or
damage to the olfactory epithelium may all compromise the success of the
intervention. Kimmelman (Kimmelman,
1994) reported a risk of 1.1% of becoming anosmic after nasal
surgery [compare Damm et al. (Damm et al., 2001)]. However,
a number of other researchers did not see a post-operative decrease in
olfactory acuity (Elwany and Harrison,
1990; Ophir et al.,
1986; Friedman et
al., 1999), indicating that the risk to olfaction from nasal
surgery is low.
|
Conclusions |
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Effective treatment of SND-related olfactory loss is possible, although not always successful. Apart from surgical approaches and/or treatment with antibiotics, both systemic and topical steroids are effectively used in the therapy of SND-related olfactory loss. In most cases an improvement in olfactory function appears to relate to the anti-inflammatory actions of the steroids used. While some details of therapeutic effect and dose regimen are not clear, systemic steroids are often helpful even in patients without nasal obstruction due to polyps or obvious inflammatory changes.
|
Acknowledgments |
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The present manuscript resulted from a session on `clinical aspects of olfaction' held during the ECRO meeting 2000 in Brighton, UK.
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TopAbstractIntroductionCauses of SND-related olfactory...Frequency of SND-related...Subjective symptomsObjective symptomsTherapy of SND-related olfactory...ConclusionsReferences |
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Accepted May 25, 2002
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