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IMAGING IN RHINOLOGY
Miscellaneous Benign Sinonasal Entities
Antrochoanal polyps are usually isolated lesions which ll the maxillary antrum and
•
extend through the (usually accessory) ostium into the middle meatus.
Inammatory sinonasal polyps are usually multiple and are seen to be crowded in the
•
nasal vault with potential bony remodelling and demineralisation. ey are associated
with atopy and aspirin intolerance.
Silent sinus syndrome is due to obstruction of the ostiomeatal complex with opacica-
•
tion of the sinus and retraction of the walls (as opposed to sinus hypoplasia where the
walls are straight). ere is a characteristic clinical presentation of hypoglobus.
Mucoceles are most frequently demonstrated in the frontal sinus with complete opaci-
•
cation and expansion or wall thinning.
An odontogenic cause may be present in 20% of ma xillary sinusitis. Odontogenic cysts
•
or tumours should be considered in the context of the opacied maxillary sinus when
a ‘double line’ of calcication is seen at its periphery.
Sinonasal Neoplasms
Whilst biopsy will usually be required for denitive diagnosis, imaging plays a role in
•
alerting the clinician to those occasions when biopsy would be ill advised (e.g. cephalocele, highly vascularised tumours, aneurysm).
All eorts should be made to perform biopsy aer imaging as bleeding or inamma-
•
tion may confound ndings.
Diagnostics should include CT and MRI.
•
Benign Sinonasal Tumours
Inverting Papilloma
A unilateral mass most commonly originating in the lateral nasal wall and involving
•
middle meatus and maxillary sinus.
CT features include internal calcication, and bony erosion or bowing. A focal bony
•
spur may correlate with the origin of this neoplasm and its identication is important
for surgical planning.
On MRI there is a characteristic convoluted, cerebriform pattern.
•
Vascular Lesions
ese include haemangioma, haemangiopericytoma, angiomatous polyp and the
•
juvenile nasal angiobroma (JNA). Vascular nature may be indicated by the nding of
ow voids and avid enhancement.
e location of the lesion is an important feature of the JNA, which characteristically
•
expands and erodes the sphenopalatine foramen.
Bone and Cartilage Tumours
Osteomas are typically found in the frontoethmoid region, and they appear as dense
•
cortical bone but may have lower density elements. Fibro-osseous lesions (brous dysplasia or ossifying broma) are usually recognisable on CT due to typical groundglass elements.
Malignant Sinonasal Tumours
Imaging Appearances
e more aggressive malignant sinonasal tumours, such as the common sinonasal
•
carcinoma and aggressive neuroendocrine tumours (e.g. SNUC- Sinonasal Un dierentiated Cancer and SNEC- Sinonasal Neuroendocrine Carcinoma), demonstrate frank
bony erosion without bony remodelling or displacement on CT.
Adenoid cystic carcinoma has a propensity for perineural spread.
•
158 Rhinology and Facial Plastic Surgery
IMAGING IN RHINOLOGY
Sinonasal melanoma is rare but melanotic forms may demonstrate high signal on
•
T1-weighted images.
T-cell lymphomas characteristically aect the nasal septum whilst B-cell lymphomas
•
arise more laterally and may demonstrate tumour on either side of the maxillary
sinus wall.
Olfactory neuroblastomas tend to arise in the superior nasal fossa and may be associ-
•
ated with peritumoural cysts when extending into the anterior cranial fossa.
Staging
MRI is particularly useful to delineate the intrasinus extent of tumour relative to
•
(increased T2w signal) inammatory change and obstructed secretions. Extrasinus
extension to the intracranial compartment, orbit and infratemporal fossa is
dened.
In particular, pial enhancement, nodular dural enhancement and dural thickening
•
of more than 5mm have been found to be predictive of dural invasion whilst brain
parenchymal signal abnormality suggests brain invasion.
Table 29.1 Approach to analysing a CT scan for inammatory disease and anatomical variants
Comment Variants
Coronal Maxillary sinus -Extent of soft tissue thickening
and density
-Bony thickening/thinning
-Mucoperiosteal calcication
Ostiomeatal
complex
Nasal cavity -Polyps
Anterior skull
base
Sphenoid sinus -Extent of disease and density
Sagittal Frontal sinus -Extent of soft tissue thickening
Sphenoethmoid
junction
Axial Ethmoid sinuses -Extent of soft tissue thickening
Sphenoid sinus -Extent of disease and density
Extrasinus soft
tissues
-Soft tissue obstruction Lateralised uncinate
-Diffuse soft tissue thickening
(note nasal cycle)
-Skull base defect Low skull base or asymmetric
-Degree of pneumatisation
and density and obstruction of
frontal sinus drainage
-Extent of soft tissue thickening
and density and obstruction of
sphenoethmoid recess
and density
-Medial orbital wall defects
-Dental disease
-Nasopharynx
-Intracranial/skull base/orbital/
deep face
Hypoplasia
Patterns of uncinate attachment
Infra-orbital air (Haller) cell
Deviated nasal septum and spurs
Concha bullosa
Paradoxical turbinate
(Keros classication)
Anterior ethmoidal artery canal
position and dehiscence
Optic nerve canal and carotid
dehiscence
Onodi (sphenoethmoid) cells
Frontoethmoid cells and agger
nasi cells
Onodi (sphenoethmoid) cells
Rhinology and Facial Plastic Surgery 159
IMAGING IN RHINOLOGY
Table 29.2 Pearls and pitfalls
CT
Isolated sinus opacication Consider a neoplasm, fungal
disease or (in the maxillary
sinus) an odontogenic source
Isolated nasal polyp Consider a cephalocele if
extending to anterior skull
base
Bony attenuation of sinonasal
structures
MRI
T1w high signal Usually due to proteinaceous
T2w high signal Usually inammatory although
Gadolinium enhancement Useful to delineate extent of
Maybe due to pressure
de-ossication from benign
disease or bony erosion from
aggressive disease
secretions (e.g. in a
mucocele). Also, due to
haemorrhage (or rarely
melanoma)
occasionally can be seen in
tumours (e.g. salivary gland
tumours or chondroid
tumours)
tumours and to assess
intracranial and perineural
spread
Correlate with endoscopic
appearances and possibly
MRI
Consider MRI prior to biopsy
Look for any evidence of
bony remodelling or
expansion which indicates
benign process such as
mucocele or polyps. Some
thin structures (such as the
anterior skull base) may be
poorly seen if there is
adjacent soft tissue
Always look at pre and post
gadolinium sequences to
distinguish high T1w
proteinaceous secretions
from enhancement
T2w is a useful sequence to
distinguish high T2 signal
inammation from the
extent of intermediate T2w
signal (cellular) tumours.
Note that very low T2w
signal is seen in benign
fungal disease
Note that enhancement due to
dural inammation or
physiological perineural
enhancement should not be
confused with tumour invasion
Post-contrast MRI sequences are particularly helpful to eva luate for perineural spread.
•
High-resolution T2w signal coronal images are useful to dene invasion since they
•
delineate the periosteum and periorbita.
CSF Leaks
CSF rhinor rhoea may be traumat ic (including post-surg ical), or non-traumatic (tumou rs,
•
infections or congenital lesions and in the setting of intracranial hypertension).
In most cases, non-contrast CT of the skull base is the only imaging investigation
•
required to identify a skull base defect.
MRI may demonstrate associated pathologies such as tumours. Heavily T2-weighted
•
thin section imaging (e.g. Constructive Interference in Steady State (CISS), Fast Imaging
Employing Steady-state Acquisition (FIESTA) may demonstrate dural defects and associated cephaloceles.
CT cisternography may be helpful if there are multiple bony defects, to dene the
•
dural breach, however, it is rarely successful in the absence of active leakage.
MR cisternography using intrathecal gadolinium is not widely available (partly due to
•
a lack of FDA approval).
160 Rhinology and Facial Plastic Surgery
ABNORMALITIES OF SMELL
30. ABNORMALITIES OF SMELL
Introduction
Although commonly overlooked by medical professionals and laypersons alike, the sense
of smell is critical for quality of life, as well as safety from such environmental hazards as
leaking natural gas, pollution and spoiled foods. Importantly, decreased smell function is
common in later life and can be an early sign of such neurodegenerative conditions such
as Alzheimer’s and Parkinson’s disease. Independent of such diseases, older persons who
cannot smell are three times more likely than their normosmic counterparts to die over the
course of the ensuing half decade.
is chapter briey summarises important aspects of olfactory anatomy and physiology,
common olfactory disorders encountered in clinical practice and practical techniques for
the evaluation and management of smell disturbances.
Anatomy and Physiology
e pseudostratied olfactory neuroepithelium harbours the 6–10 million ciliated olfactory
receptor cells critical for smell function. It lines the cribriform plate and sectors of the superior turbinate, middle turbinate and septum in the upper recesses of the nose. e olfactory
receptor cell axons traverse the cribriform plate and pia matter via 30–50 fascicles, termed
the olfactory la. Because of their direct projection into the olfactory cle without an intervening synapse, the receptor cells can serve as a conduit for the movement of viruses and
other exogenous agents from the environment into the brain. is was recognised many
years ago for the poliovirus, leading to public health programs to chemically cauterise the
olfactory epithelium of school children with zinc sulfate to avert contracting polio during
epidemics in the 1930s.
The incoming olfactory receptor cell axons synapse with second-order neurons within
distinct spherical olfactory bulb structures termed glomeruli. A considerable amount
of convergence of information occurs within the glomeruli, from which projection neurons, the mitral and tufted cells, send processes directly to higher structures such as
the anterior olfactory nucleus, the piriform cortex, the entorhinal cortex and amygdala
without first synapsing within the thalamus. Reciprocal interactions occur among such
structures.
Clinical Evaluation of Smell Function
Proper assessment of a patient’s smell function requires a detailed clinical history and a thorough physical examination including appropriate brain and sinonasal imaging. e latter
may include a computed tomography (CT) or of the paranasal sinuses to evaluate conductive smell disturbance such as nasal polyps or a lesion, and a magnetic resonance imaging (MRI) of the paranasal sinuses and brain to examine sensorineural impairment. Other
tests include objective olfactory, and in some cases, taste testing. It is important to recognise
that patients frequently confuse ‘taste problems’ with true smell loss, and that many deny
any olfactory disturbance until formal testing proves otherwise. Self-administered olfactory tests are commercially available, making accurate testing practical without having to
otherwise tie up clinic resources. e most popular of these tests is the 40-item University
of Pennsylvania Smell Identication Test (UPSIT; Figure 30.1), which is a test that provides
an accurate indication of not only absolute dysfunction (e.g. anosmia or mild, moderate or
severe microsmia), but a percentile rank relative to a patient’s age and sex and an index of
probable malingering (Figure 30.1).
A number of questions should be made during a patient’s evaluation. What is the timing of
onset, duration of impairment and pattern of occurrence? Sudden olfactory loss can be consistent with possible head trauma, ischaemia, infection or a psychiatric condition. Gradual
Rhinology and Facial Plastic Surgery 161
ABNORMALITIES OF SMELL
Figure 30.1 The four booklets of the 40-odorant University of Pennsylvania Smell Identication
Test (UPSIT; commercially known as the Smell Identication TestTM). Each page contains a microencapsulated odorant that is released by means of a pencil tip. This test, which has been administered to ˜1,000,000 patients since its development, is the most widely used olfactory test in the
world, with multiple language versions available. The UPSIT is considered to be the ‘eye chart for
the nose.’ (Photo courtesy Sensonics International, Haddon Heights, NJ 08035 USA. Copyright ©
2000 by Sensonics International.)
loss may indicate a progressive and obstructive lesion in or around the sinonasal region,
particularly if the loss is unilateral. Intermittent loss may suggest an inammatory process
in association with nasal and sinus disease. Is there a history of precipitating antecedent
events, such as head trauma, viral upper respiratory infections, chemical or toxin exposures
or sinonasal surgery? Does the patient have any nasal discharge that is mucous appearing
(e.g. allergy), purulent (e.g. infection) or clear (cerebrospinal uid [CSF] rhinorrhoea aer
trauma)? Does the patient use drugs, such as intranasal cocaine, ethanol or tobacco? Each
of these substances has been associated with some form of olfactory impairment. Cigarette
smoking results in a loss of olfactory ability that is proportional to the cumulative smoking
dose. Cessation of smoking can result in improvement in olfactory function over time. Are
there any medications that the patient is taking that might compromise function? Awareness
of pending litigation and the possibility of malingering should be considered since olfactory
loss is a compensable injury.
Causes of Smell Disturbance
In general, loss of olfactory function can be subdivided into two classes:
Conductive or transport impairments from obstruction of the nasal passages (e.g.
•
chronic nasal inammation, polyposis, etc.)
Sensorineural impairment from damage to the olfactory neuroepithelium, central tracts
•
and connections (e.g. viruses, airborne toxins, tumours, seizures, etc.)
In some circumstances, both can be involved. Chronic rhinosinusitis, for example, can produce damage to the olfactory membrane in addition to blocking airow, and altered membrane function can, over time, lead to degeneration within the olfactory bulb, which is a
central structure. Although many causes of olfactory disturbance due to conductive factors
162 Rhinology and Facial Plastic Surgery
ABNORMALITIES OF SMELL
Table 30.1 Reported agents, diseases, drugs, interventions and other etiologic categories
associated in the medical or toxicologic literature with olfactory dysfunction
Air pollutants and industrial dusts
Acetone, benzol, chlorine, formaldehyde,
silicone dioxide
Drugs
Adrenal steroids (chronic use)
Analgesics (antipyrine)
Anaesthetics, local (cocaine HCl, procaine HCl,
tetracaine HCl)
Anticancer agents (e.g. methotrexate)
Antihistamines (e.g. chlorpheniramine malate)
Antimicrobials (lincomycin, macrolides,
penicillin, tetracyclines)
Antirheumatics (e.g. mercury/gold salts)
Antithyroids
Antivirals
Cardiovascular/hypertensives
Gastric medications (e.g. cimetidine)
Hyperlipoproteinemia medications (e.g.
cholestyramine)
Psychopharmaceuticals (e.g. LSD, psilocybin)
Sympathomimetics (e.g. amphetamine sulfate)
Note: This is a shortened table with examples per category. Full table can be found in the Scott-
Brown Textbook.
Lesions of the nose/airway blockage
Inammatory diseases, structural abnormalities,
nasal masses
Medical Interventions
Intracranial/sinonasal procedures,
radiotherapy
Neurologic
Alzheimer’s disease, Down’s syndrome, head
trauma, meningitis, Parkinson’s disease,
syphilis
Nutritional/metabolic
Chronic alcoholism, gout, vitamin deciency
Endocrine/metabolic
Addison’s disease, Cushing’s syndrome,
diabetes mellitus, Kallmann’s syndrome
Pregnancy, panhypopituitarism,
pseudohypoparathyroidism
Psychiatric
Anorexia nervosa, depressive disorder,
schizophrenia
or inammation of the olfactory epithelium can be treated, most olfactory disorders due to
sensorineural factors remain untreatable.
A listing of the causes of olfactory dysfunction that have been reported in the medical
literature is presented in Table 30.1. e three most more common disorders or entities
associated with olfactory impairment are head trauma, chronic rhinosinusitis and upper
respiratory infections, such as those due to the common cold, inuenza, bacterial infections and, more recently, infection with the SARS-CoV-2 (COVID-19) virus. Cumulative
damage over time can occur, such that persons are predisposed for signicant loss later
in life as a result of prior nasal infections and exposures to air pollutants that induce
subclinical damage.
Treatment of Smell Disorders
The most effective treatments available are those for conductive anosmia, where inflammation and other factors obstruct movement of molecules to olfactory receptors.
Conductive and sensorineural olfactory loss are often distinguishable using a brief
course of systemic steroid therapy since patients with conductive impairment often
respond positively to the treatment, although long-term systemic steroid therapy is not
advised. Increased topical efficacy can occur when the nasal drops or spray are administered in the head-down Moffett position. Proper allergy management is essential and
may require the use of an antihistamine. When a bacterial infection is suspected (e.g.
infectious sinusitis), a course of antibiotics should be used. Importantly, pre- and postintervention olfactory testing should be performed to establish intervention efficacy, as
well as to screen for subsequent slow relapse that is characteristic of most conductive
disorders.
Sensorineural impairment of olfaction is typically more dicult to manage, and the prognosis for patients suering from long-standing total loss due to upper respiratory illness
Rhinology and Facial Plastic Surgery 163
ALLERGIC RHINITIS
or head trauma is poor. e majority of patients who recover smell function subsequent to
trauma do so within 12 weeks of injury, although in rare cases return can occur over a several
year period. Patients who quit smoking typically have dose-related improvement in olfactory
function and avour sensation over time. Central lesions, such as central nervous system
(CNS) tumours that impinge on olfactory bulbs and tracts can oen be resected with signicant improvement in olfactory function. Patients with neurological conditions such as
epilepsy, migraine or multiple sclerosis should be treated appropriately with specialist input.
If there is depression or psychosis a psychiatric referral is indicated.
Practicing smelling odours (olfactory training) before and aer sleeping may be helpful in
returning function, but careful double-blind studies with adequate controls are lacking.
ere is some evidence to support administration of antioxidants such as alpha-lipoic acid.
Spontaneous recovery depends on severity of disturbance. Literature reports that only 11%
of anosmic and 23% of microsmic patients regain normal age-related function over time.
Olfactory training involves at least four odours of separate categories (typically oral, rose;
fruity, lemon; aromatic, eucalyptus and resinous, clove; patients are advised to sni these for
15 seconds at least twice a day, for up to 6 months.
In patients with complete anosmia, supportive measures are necessary to protect them from
further harm:
Smoke and carbon monoxide detectors need to be installed and properly working.
•
Electric stoves should be used instead of gas.
•
Expirations dates for food products should be checked.
•
Balanced diet to prevent weight loss and malnutrition (particularly in the elderly).
•
Adding avour enhancers (e.g. monosodium glutamate, food colouring, chicken or
•
beef stock) to foods can also help with their appeal.
31. ALLERGIC RHINITIS
Introduction
Allergic rhinitis (AR) is characterised by inammatory changes in the nasal mucosa caused
by exposure to an inhaled allergen to which an individual has become sensitised (a type I
hypersensitivity reaction in the Gell and Coombs classication).
In the preparation phase (sensitisation), the allergen is processed by dendritic cells and presented to T-helper 2 cells (TH2). TH2 cells release interleukins (IL-4, IL-5, IL-13 and others)
that promote B-cell dierentiation into plasma cells producing immunoglobulin E (IgE),
which binds to mast cells receptors. Memory B cells are formed from activated B cells and
are specic to the antigen encountered during the sensitisation.
On subsequent interaction with the antigen (primary phase), cross-linking of IgE results in
degranulation of mast cells. is triggers the release of inammatory mediators, including
histamine and leukotrienes, resulting in the classic symptoms of AR.
During the late phase, inammatory cells (mast cells, eosinophils, T cells and others) inltrate mucosa, resulting in increased and persistent symptoms. Repeated interaction with the
same allergen stimulates mast cells more quickly.
AR is part of a systemic disease process termed the unied allergic airway that involves other
organs such as the lungs with allergic asthma and the eyes with allergic conjunctivitis.
164 Rhinology and Facial Plastic Surgery
ALLERGIC RHINITIS
Intermittent symptoms
<4 days per week
or <4 consecutive weeks
per year
Mild
Normal sleep
Normal daily activities
Normal work and school
No troublesome symptoms
Figure 31.1 Classication of allergic rhinitis. (Reproduced with permission of authors, Bousquet
et al., 2008.)
Persistent symptoms
>4 days per week
AND >4 consecutive weeks
per year
Moderate–severe
One or more items
Abnormal sleep
Impairment of daily activities,
sport, leisure
Problems caused at school or
work
Troublesome symptoms
Denition
AR is subdivided into intermittent AR (IAR) and persistent AR (PER), and the severity into
mild, moderate or severe (Figure 31.1).
Other causes of rhinitis may have similar symptoms, but allergic disease can be diagnosed by
correlating typical symptoms with diagnostic tests such as skin prick tests or measurement
of specic IgE levels in the blood.
Prevalence
e prevalence of allergic disease varies around the world from 0.8–39.7% of the population.
Disease prevalence has increased signicantly in western society over the last 50 years to
23%, possibly caused by reduced exposure to infectious microbes or to reduced infestation
with worms in the gut, which appear to exert a regulatory eect on the immune system.
Natural History
Having parents who are atopic increases the risk of atopy in their children by 3- to 6-fold,
but exposure to allergens also plays a role. e term ‘atopic march’ refers to the sequential
development of allergic disease, starting with infantile atopic eczema, then the development
of AR and nally allergic asthma. Conversely, AR oen becomes less severe with age and
skin prick testing shows reduced reactivity in the elderly.
Presentation and Diagnosis
AR typically presents with two or more of the following symptoms: anterior or posterior
rhinorrhoea, sneezing and nasal block and/or itching. Other symptoms include itchy eyes,
pharyngeal itch, reduced smell, cough and sore throat.
Nasal blockage may also result in a reduced quality of life, sleep disorders, learning and
attention impairment, mouth breathing and malocclusion.
Unilateral symptoms, purulent discharge, epistaxis and pain are not typical of AR and
should prompt further investigation.
e timing of symptoms and their severity will allow the disease to be classied. For example, symptoms worse in the morning may suggest house dust mite sensitivity from exposure
in bed or symptoms that occur in the spring may indicate tree pollen sensitivity. If the allergen driving the AR is unclear from the history, then skin prick testing or measurement of
specic IgE levels can be undertaken to clarify this.
Rhinology and Facial Plastic Surgery 165
ALLERGIC RHINITIS
Treatment
Allergen Avoidance
Allergen avoidance can be dicult to achieve or may be relatively ineective, but measures
such as using anti-allergy covers on mattresses and pillows can be tried in patients with
house dust mite sensitivity. Keeping pets out of the bedroom is also advised in patients with
dog or cat allergy.
Pharmacological Treatments
e mainstay of drug treatment in AR involves the use of oral and topical antihistamines and
topical corticosteroids. e basic summary of recommendations for treatment according to
the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines
1
is shown in Fig ure 31.2.
Oral and topical antihistamines are rapid acting and reduce symptoms of sneezing and itch
but are less eective at improving the airway. Topical (and occasionally systemic) corticosteroids are slower acting but have a greater eect on reducing blockage. Combined intra-nasal
uticasone propionate and azelastine hydrochloride in a single device is more eective than
Intermittent
symptoms
Mild
Not in preferred order:
oral H
blocker or
1
intranasal H1 blocker
and/or decongestant
or LTRA
Diagnosis of allergic rhinitis
Persistent
symptoms
Moderate-
severe
Not in preferred order:
oral H
intranasal H
and/or decongestant
or intranasal CS
or LTRA (or cromone)
In persistent rhinitis
review the patient
after 2–4 weeks
If failure: step-up
If improved: continue
for 1 months
blocker or
1
1
Mild
blocker
Allergen and irritant avoidance may be appropriate
Check for asthma, especially in
patients with severe and/or
persistent rhinitis
Moderate-
severe
In preferred order:
intranasal CS
H1 blocker or LTRA
Review the patient
after 2–4 weeks
Improved
Step-down
and continue
treatment
for >1 month
Add or increase
intranasal CS
dose
If conjunctivitis
Add
oral H1 blocker
or intraocular H
or intraocular cromone
(or saline)
Failure
Review diagnosis
Review compliance
Query infections
or other causes
Rhinorrhea:
add ipratropium
blocker
1
Blockage: add
decongestant
or oral CS
(short term)
Failure:
referral to specialist
Consider specific immunotherapy
Figure 31.2 Allergic rhinitis management. CS, corticosteroids; LTRA, leukotriene receptor antago-
nist. (Reproduced with permission of authors, Bousquet et al., 2008.)
166 Rhinology and Facial Plastic Surgery
ALLERGIC RHINITIS
Table 31.1 Pharmacological treatments and their effects in allergic rhinitis
Itch/sneezing Discharge Blockage Impaired smell
Sodium cromoglicate + + +/– –
Oral antihistamines +++ ++ +/– –
Ipratropium bromide – +++ – –
Topical decongestants – – +++ –
Topical corticosteroids +++ +++ ++ +
Oral corticosteroids +++ +++ +++ ++
Antileukotrienes – ++ + +/–
Combined topical steroid and
antihistamine
Note: – No effect; + marginal effect; +++ substantial effect.
+++ +++ +++ ++
monotherapy and is indicated for patients when monotherapy with either an intra-nasal
H1-antihistamine or glucocorticoid is considered inadequate.
Leukotriene receptor antagonists such as montelukast can be useful in some patients, particularly those with asthma or who develop wheeze at the peak of the pollen season.
Ipratropium topical spray can be useful if rhinorrhoea is a particular problem and can be
used as an adjunct to a steroid spray.
Nasal douching with saline may be eective in physically removing allergens from the nose
and is safe and easy to perform.
A summary of the eects of the common drugs used to treat AR is noted in Table 31.1.
Anti-IgE humanised monoclonal antibodies may increasingly play a role in allergic disease
modication. Licensed drugs such as omalizumab bind to and reduce levels of active circulating IgE and therefore reduce symptoms, but they are expensive and must be given by
injection. Newer drugs such as dupilumab (an IL-4 receptor antagonist) are being developed
that can target specic cytokines and may allow a more patient-specic therapy with fewer
side eects than current treatment options.
Immunotherapy (desensitisation) is a method of inducing tolerance to an allergen and
therefore a reduction in symptoms with exposure. Treatment may be given by injection
(subcutaneous immunotherapy [SCIT]) or sublingually (sublingual immunotherapy
[SLIT]). erapy involves exposing the patient to the allergen to which they have become
sensitised, usually in gradually increasing doses. Immunotherapy is usually reserved for
patients who have had poor symptom control with standard treatment and in carefully
selected patients can be very eective. Treatment is normally continued over 3 years, which
causes a modication of the immune system, and long-lasting symptom control may be
achieved following cessation of treatment. It has a risk, however, of causing anaphylaxis and
patients should be monitored for 30–60 minutes following each injection (SCIT). SLIT can
safely be taken by the patient at home if the rst dose has been monitored and a minimal
reaction has occurred.
Children with AR
AR is the most prevalent allergic disease in children and may have signicant eects on their
quality of life. e treatment algorithm for children is broadly similar to that for adults.
Avoidance measures then, if necessary, and an oral non-sedating antihistamine are the rstline therapies, but a trial of a leukotriene receptor antagonist may be considered in children
who are already using an inhaled steroid for asthma, or if a topical steroid is not tolerated.
Fluticasone (licensed from age 4 years) or mometasone (licensed from 6 years) have low systemic bioavailability and are the topical corticosteroids of choice.
Rhinology and Facial Plastic Surgery 167
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