Evidence-based management of a patient with anosmia
Geyer, M. & Nilssen, E.
Department of Otorhinolaryngology, Head and Neck Surgery, Queen Alexandra Hospital, Cosham, Portsmouth,
Hampshire PO6 3LY, UK
A 52-year-old female comes to the out patient clinic with
a 4-month history of anosmia and reduced taste.
Anosmia is defined as loss or absence of the sense of
smell. It is a common condition and affects approxi-
mately 1% of the population under age 60 years.
1
Olfac-
tory function also decreases with aging.
2–4
Abnormalities
of olfaction include: (i) anosmia (inability to detect
odours), (ii) hyposmia (diminished olfactory sensitivity)
and (iii) dysosmia (distorted identification of smell),
which includes (a) parosmia (altered perception of smell)
and (b) phantosmia (smelling non-existent odours).
5
Loss
of smell often manifests as a loss of taste. In addition,
cranial nerves V, IX and X sense noxious stimuli.
6
Disorders of smell may be broadly classified into three
groups: (i) conductive (transport) loss: conditions that
interfere with access of the odorant to the olfactory neu-
roepithelium, (ii) sensory loss: injury to receptor region
or (iii) neural loss: damage of central olfactory pathways.
7
The three most common causes of olfactory disorders
are: (i) sinonasal disease (
25%), (ii) postviral anosmia
(
20%) and (iii) head trauma (15%).
What should you cover in the history
A thorough history will provide important clues as to the
aetiology and is a cornerstone of making a correct diag-
nosis.
8
1 Onset. A viral upper respiratory tract infection precedes
the onset of anosmia in around 20% of patients. Postviral
anosmia is more common in those over 40 years and is
usually reported within 6 months of the infection.
9
Head
trauma is complicated by anosmia in 15% of cases, and is
usually of immediate onset, but often only recognised
once the patient recovers from their head injury. How-
ever, of all head trauma cases, only 0.5–5% present with
anosmia. Shearing force on olfactory filaments, olfactory
bulb contusion and frontal lobe injury are proposed
potential causative mechanisms.
10
The degree of olfactory
loss may be associated with severity and site of cranial
trauma. An occipital blow is commonly implicated.
2 Duration. Spontaneous return of function is known to
occur if anosmia or hyposmia has been present for
<2 years after a viral infection or head trauma. If present
for longer than 2 years the condition is likely remain
permanently.
11
3 Nature of the disorder of smell. In postviral cases, hy-
posmia or dysosmia are more likely to occur than anos-
mia. This is typically either a constant foul smell or a
distortion of normal smell.
12,13
4 Related sinonasal disease. Twenty to 30% of patients
have nasal and sinus disease, most commonly polyp dis-
ease,
14
chronic rhinosinusitis
15
or allergic rhinitis.
16
Sino-
nasal disease is the most treatable aetiology of anosmia.
Although nasal obstruction of the olfactory cleft, second-
ary to nasal mucosal swelling, polyps, bony deformities
and rarely tumours can result in anosmia, olfactory sensi-
tivity does not correlate with nasal patency alone.
5 Episodic improvement and previous olfactory dysfunction.
Patients with episodic loss may be more likely to recover
function, and may benefit from topical nasal treatment.
6 Associated otorhinolaryngological symptoms. Complaints
such as epistaxis, nasal obstruction, an enlarging neck
mass or focal neurological deficits are important warning
signs and symptoms and should alert the physician to a
possible neoplastic cause, such as an aesthesioblastoma or
meningioma, though often these tumours remain silent
and often present late.
7 Taste loss. Two-thirds of patients complain of taste loss
but only few actually have taste changes identified by test-
ing. Thus, most patients have normal taste thresholds.
17,18
However, 67% have objective changes of their sense of
smell and complain of a loss of flavour detection, which
is mainly an olfactory function.
8 Medical conditions. Systemic disease such as endocrine
disturbances (e.g. hypothyroidism, diabetes mellitus) and
neurological conditions (e.g. temporal lobe epilepsy and
schizophrenia)
19
may present with disorders of olfaction.
9 Smoke and chemical exposure. Exposure to cigarette
smoke and other toxic chemicals can cause damage to the
olfactory epithelium. Examples of agents associated with
olfactory dysfunction include organic compounds (e.g.
acetone, benzene, ethyl acetate), industrial agents (e.g.
paint solvent), dusts (e.g. cement), metals (e.g. lead, zinc,
mercury) and inorganic compounds (e.g. ammonia, car-
bon monoxide). Spontaneous recovery can occur if the
insult is discontinued.
20
A
1
2
M
INUTE
C
ONSULTATION
Ó 2008 The Authors
466
Journal compilation Ó 2008 Blackwell Publishing Ltd
•
Clinical Otolaryngology 33, 466–469
10 Medications. Anosmia is a complication of many med-
ications and therefore a drug history is important. Com-
mon medications to ask about include antidepressants
(e.g. Amitriptyline), antihypertensives (e.g. Enalapril,
Nifedipine, Propranolol), anti-inflammatory agents (e.g.
Penicillamine), antimigraine agents (e.g. Sumatriptan),
antineoplastics (e.g. Cisplatin), antipsychotics (Trifluoper-
azine), and antithyroid agents (Propylthiouracil).
21
What should you cover on examination
Meticulous physical examination is essential and should
include a full ENT examination as well as a careful neu-
rological evaluation as appropriate.
1 Nasal examination. Rhinoscopy is the cornerstone of
assessment. Anterior rhinoscopy in the non-decongested
nose should be supplemented with post-decongestant flexi-
ble endoscopy of the nasal cavity, postnasal space, pharynx
and larynx. Inflammation, mucopurulent discharge, polyps
and masses are indicative of an underlying pathology.
2 Otoscopy. Serous otitis media suggests the presence of a
nasopharyngeal mass or inflammation.
3 Neck. Palpate for pathologically enlarged lymph nodes.
4 Neurological examination. Carefully examine all cranial
nerves where appropriate and look for signs of raised
intracranial pressure such as papilloedema.
5 Sensory evaluation. Assessment of olfactory function
corroborates
the
patient’s
complaint,
evaluates
the
efficacy of treatment and determines the degree of
permanent impairment.
22
Although many testing kits
are available, it is our experience that outside major
centres they are still not used widely in the clinical
setting, and considerable variation is present in the
reliability of olfactory tests.
23
• Determining qualitative sensations by smell testing
(odour identification tests). There are a variety of
commercially available olfactory tests. The University
of Pennsylvania Smell Identification Test (UPSIT) is
an example of such a test.
24
The UPSIT involves 40
microencapsulated odours in a scratch-and-sniff
format, with four forced choice response alternatives
accompanying each odour. The scores are compared
against sex- and age-related norms. Anosmic patients
score at or near chance (10 ⁄ 40 correct). Malingering
occasionally occurs, and should be considered in
patients scoring 5 or less. The UPSIT test-retest
reliability is high (r
¼ 0.92).
24,25
• Determining the detection threshold. By using successive
dilutions of phenylethyl alcohol (PEA) detection
thresholds can be established
26
(r
¼ 0.88).
24
The
‘Sniffin’ Sticks’ system uses n-butanol pen-like odour
dispensing devices that contain different concentrations
of
odours.
27
Threshold
testing
by
olfactory
evoked response measurement is used in the research
setting.
28
What management should you offer
1 Laboratory investigations. Based on history and physical
examination, tests to exclude renal, hepatic and various
endocrine disorders may be obtained. They are not other-
wise recommended as routine tests. Allergy testing as
appropriate should also be considered.
2 Biopsy. Olfactory epithelium biopsy is generally not
undertaken except in the research setting.
29
3 Radiological investigations. CT and MRI imaging may
be ordered if indicated by the history and examination.
30
• CT scan: Patients with signs and symptoms of sino-
nasal disease should be treated in the usual way. If
they fail to respond to appropriate treatment then
they would undergo imaging as part of their subse-
quent management. Patients with sinonasal symptoms
but without any obvious pathology found on examina-
tion should also undergo a scan of the paranasal
sinuses as part of the evaluation of their symptom
complex. This identifies a group of patients who may
benefit from either further medical and ⁄ or surgical
intervention if an abnormality is confirmed on imag-
ing.
31
The CT scan will also include views of the cribri-
form plate and anterior skull base and may provide
evidence of local bone erosion or destruction, but will
not readily pick up intracranial soft tissue disease.
• MRI scan: Patients without evidence of sinonasal dis-
ease on history or examination should have an MRI
scan of the brain to exclude a sensorineural cause for
their anosmia. This will exclude uncommon tumours
of the anterior cranial fossa and brain, such as menin-
giomas, aesthesioblatomas, and craniopharyngiomas.
32
1 Conductive (transport) olfactory loss
Treatment of sinonasal conditions should be evidence
based, as provided by the recently updated EPOS docu-
ment,
33
as well as other relevant literature, beyond the
scope of this article.
34
Briefly, topical nasal steroids have
been shown to have some benefit in certain trials.
22
Other
modalities include a short course of oral steroids, antibi-
otics, hyposensitisation and surgery where appropriate.
35
Furthermore, a short course of oral steroids may help to
diagnose reversible conductive loss.
2 Sensorineural olfactory loss
• Few of the sensorineural olfactory defects have
specific treatments. Traumatic and postviral anosmia
should be treated expectantly, accepting that no
specific treatment is proven to lead to a resolution of
symptoms.
36
Patient reassurance and education is
A 12 minute consultation
467
Ó 2008 The Authors
Journal compilation Ó 2008 Blackwell Publishing Ltd
•
Clinical Otolaryngology 33, 466–469
vital. Steroids may be used in an attempt to reduce
inflammation in cases of viral illness, sarcoidosis and
multiple sclerosis.
• There is scanty evidence confirming the efficacy of
treatment of idiopathic sensorineural olfactory loss.
Zinc sulphate is best known, but appears unsuccess-
ful.
37
Vitamin therapy also has no proven benefit.
38
• Rare tumours of the anterior cranial fossa are treated
by neurosurgical, radiotherapy and chemotherapy
intervention as indicated.
3 Smoking cessation. Elimination of this and other air-
borne toxins may help to restore olfactory function.
4 Patient reassurance and education. Once the relevant
investigations have proven negative the patient may be
reassured that they do not have a deleterious underlying
pathology. Unfortunately, a cure is often difficult to obtain.
The psychological and potential health impacts of disorders
of olfaction are well recognised, especially in the elderly.
Anosmia may adversely affect appetite, leading to lack of
interest in eating and malnutrition, complicated by weight
loss and a general adverse impact on health.
39,40
Hazards resulting from this disorder also need to be
highlighted. It is important to warn the patient that an
olfactory disorder will render them unable to detect cer-
tain hazards, and lifestyle adjustments may be necessary.
For example, smoke and natural gas detectors are essen-
tial to minimise risk in the home environment.
41
Patients
should also be warned to pay attention to the sell-by-date
on food to avoid eating items which are spoiled.
Search stategy
Current texts, the Cochrane library and other evidence-
based databases were searched in the preparation of this
paper. The current peer-reviewed literature was also
searched using Medline under the MeSH heading ‘anos-
mia’ and using subheadings for epidemiology, therapy,
drug therapy and surgery. The search was limited to the
English language, human studies and to clinical trials,
randomised controlled trials and meta-analyses. The
search was performed on 1 July 2008.
Conflict of interest
None to declare.
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Ó 2008 The Authors
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•
Clinical Otolaryngology 33, 466–469
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