Complications Most research still classifies allergic rhinitis according to its sea-
Pruritus is accompanied by intense scratching. Skin may thicken, sonality or its perennial nature. Seasonal allergic rhinitis is com-
displaying lichen simplex chronicus: a localized skin thickening
often appearing over the posterior neck, extremities, scrotum,
vulva, anus, and buttocks. In prurigo nodularis, a variant of lichen
simplex chronicus, some nodules develop over areas within easy
scratching reach, such as the extensor arms and legs. Impetigo
may result from superinfected excoriations in patients with atopic
dermatitis.
References
Ikoma A, Rukwied R, St€ ander S, et al: Neurophysiology of pruritus: Interaction of itch
and pain, Arch Dermatol 139:1475–1478, 2003.
St€ander S, Weisshaar E, Mettang T, et al: Clinical classification of itch: A position
paper of the International Forum for the Study of Itch, Acta Derm Venereol
87:291–294, 2007.
Zirwas MJ, Seraly MP: Pruritus of unknown origin: A retrospective study, J Am Acad
Dermatol 45:892–896, 2001.
Cho YL, Liu HN, Huang TP, Tarng DC: Uremic pruritus: Roles of parathyroid hor-
mone and substance P, J Am Acad Dermatol 36:538–543, 1997.
Ganesh E, Maxwell LG: Pathophysiology and management of opioid-induced pruri-
tus, Drugs 67:2323–2333, 2007.
Krajnik M, Zylicz Z: Understanding pruritus in systemic disease, J Pain Symptom
Manage 21:151–168, 2001.
Reamy B: A diagnostic approach to pruritus, Am Fam Physician 84:195–202, 2011.
Moses S: Pruritus, Am Fam Physician 68:1135–1142, 2003.
1 Symptomatic Care Pending Diagnosis
RHINITIS
Method of
Sheryl Beard, MD
CURRENT DIAGNOSIS
• Rhinitis presents as nasal congestion, sneezing, itching, rhinor-
rhea, and postnasal drainage.
• Patients with palatal and nasal itching should be considered for
allergic disease.
• Allergic rhinitis is confirmed by positive skin-prick testing and
IgE reactivity.
• Nonallergic rhinitis patients lack allergic evidence for disease.
54 • Nonallergic rhinitis conditions have multiple presentations.
CURRENT THERAPY
• Avoidance therapy should be first-line treatment for all forms of
rhinitis.
• Second generation oral antihistamines have good therapeutic
efficacy for allergic rhinitis.
• Intranasal corticosteroids are the mainstay of treatment for
nonallergic rhinitis and moderate-to-severe allergic rhinitis.
• Consultation with an allergy specialist should be considered in
cases with multiple treatment failures.
• Patients whose allergic rhinitis is uncontrolled on multiple
therapies should be considered for immunotherapy.
Introduction
Rhinitis is defined as inflammation of the nasal mucous membranes.
Rhinitis presents as nasal congestion, sneezing, itching, rhinorrhea,
and postnasal drainage; it can be divided into allergic and nonallergic
rhinitis. Mixed rhinitis has components of both allergic and nonaller-
gic disease. Allergic rhinitis is nasal inflammation that is mediated by
IgE to environmental allergens. Nonallergic rhinitis is defined by
non–IgE-mediated perennial symptoms. Nonallergic rhinitis shares
symptoms with allergic rhinitis, but is only distinguishable by nega-
tive allergy tests. Nonallergic rhinitis is also known as perennial non-
allergic rhinitis, idiopathic rhinitis, and vasomotor rhinitis.
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monly caused by pollen allergens; perennial allergic rhinitis is
mainly caused by dust mites and animal dander. Allergic rhinitis
can be further classified as mild, moderate, or severe. Mild rhinitis
is rhinitis that does not impair work, school, daily functioning, or
sleep. Moderate to severe rhinitis interferes with activities of daily
living, quality of life, and/or sleep. Severe rhinitis is so marked that
normal functioning cannot take place without treatment. Episodic
allergic rhinitis occurs with sporadic inhalant aeroallergen expo-
sure not typically encountered by the patient’s usual indoor and
outdoor environments. An example of episodic allergic rhinitis is
a child who is allergic to cats but is not normally exposed, but then
visits a household with cats and develops symptoms.
The Allergic Rhinitis and its Impact on Asthma Guidelines:
Revised 2010 (ARIA) discouraged the use of the terms seasonal
and perennial rhinitis in favor of intermittent and persistent rhini-
tis. Intermittent rhinitis can be defined as nasal symptoms lasting
less than 4 weeks’ duration and fewer than 4 days per week. Per-
sistent rhinitis is rhinitis lasting more than 4 weeks’ duration or
more that 4 days per week.
No standard classification exists for nonallergic rhinitis. A vari-
ety of conditions present with similar symptoms and are called non-
allergic rhinitis. Nonallergic rhinitis includes vasomotor rhinitis,
gustatory rhinitis, nonallergic rhinitis with eosinophilia syndrome
(NARES), occupational rhinitis, hormonal rhinitis, drug-induced
rhinitis, and atrophic rhinitis. Another entity classified in or out
of nonallergic rhinitis is infectious rhinitis.
Local allergic rhinitis is a newly defined entity found in nonato-
pic patients. Local allergic rhinitis is characterized by local inflam-
matory reactions including local eosinophils and localized IgE in
response to aeroallergens. Local allergic rhinitis does not show sig-
nificant skin-prick testing reactions, and patients have negative sys-
temic IgE reactions to aeroallergens.
Rhinitis may be viewed by some as a trivial disease, but it places a
significant financial burden on society. The estimated direct and
indirect costs to society of rhinitis were around $11.58 billion
in 2002.
Epidemiology/Risk Factors
The National Health and Nutrition Survey (NHANES II and III)
suggests that the overall prevalence of IgE sensitivity might be
increasing. Of the patients evaluated for rhinitis in the United
States, 43% (58 million people) have allergic disease, 23% (19 mil-
lion people) have nonallergic disease, and 34% (26 million people)
have mixed rhinitis. Seventy percent of allergic patients develop the
disease in childhood (20 years and younger) as opposed to nonal-
lergic rhinitis patients, 70% of whom develop disease in adulthood.
Approximately two thirds of nonallergic rhinitis patients have
vasomotor rhinitis, and one-third have NARES. Nonallergic rhini-
tis has a female predominance.
The prevalence of local allergic rhinitis is largely unknown. In a
small study of rhinitis patients, the prevalence of local allergic rhi-
nitis was 25.7%, nonallergic rhinitis was 11.2%, and allergic rhi-
nitis was 63.1%. Local allergic rhinitis is associated with asthma
and conjunctivitis, and commonly begins in childhood.
Pathophysiology
Allergic
Allergic rhinitis is the result of an IgE mediated, type I hypersensi-
tivity allergic reaction in response to an inhaled allergen. Allergens
are proteins derived from airborne particulate matter, including
dust-mite feces, pollens, animal dander, and cockroach particles.
Antigen-presenting cells (APCs) engulf allergens in the nose and
break them into antigenic peptides. APCs present these peptides
to naïve T cells (TH0). TH0 cells differentiate once activated, into
the TH2 subtype. The TH2 lymphocytes generate cytokines that
regulate B-lymphocytes and sequester inflammatory cells (includ-
ing eosinophils).
B-lymphocytes produce IgE. IgE attaches to mast cells and baso-
phils and renders them sensitized. Once sensitized and cells are
exposed to allergen, the mast cells and basophils degranulate.
Degranulation of these cells releases a host of mediators including
histamine and prostaglandin. Histamine stimulates histamine type
I (H1) receptors on nerve endings that cause pruritus, sneezing and
increased secretions. These symptoms constitute the early-phase
response of allergic rhinitis. The early-phase response occurs
within minutes of allergen exposure and dissipates within 1 hour.
Eosinophils produce IL-5, which acts to promote activation and
survival of other eosinophils. Eosinophils also produce toxic prod-
ucts that damage local mucosal cells. The damage done by these
cells is what constitutes the late-phase reaction. The late-phase
reaction occurs several hours after allergen exposure and is charac-
terized by nasal congestion.
Nonallergic Rhinitis
The nasal mucosa has two major functions; one is trapping inhaled
particles through mucus production and the second is humidifying
inhaled air through a complex vascular system. The mucus glands
and the vascular system are regulated by the parasympathetic and
the adrenergic nervous systems. Sensory nerves are stimulated by
irritants in the nose through the use of a sensory receptor called a
nociceptor. The nociceptive signal generates a neural reflex in the
central nervous system (CNS) controlling sympathetic and parasym-
pathetic tone in the nasal mucosa. Parasympathetic stimulation
results in mucus production. Sympathetic stimulation causes vaso-
constriction, which empties venous cavities. Lack of sympathetic
tone causes venous engorgement and nasal congestion.
Symptomatic nonallergic rhinitis is an exaggeration of a normal
defensive mechanism. Inflammation in the nose causes an upregu-
lation of this neural activity, resulting in the exaggerated response
(also known as neural hyperresponsiveness). Hyperresponsive
parasympathetic efferent nerves trigger glandular activation in
the nasal mucosa, leading to vasodilation and mucus production.
Excessive mucus production anteriorly causes rhinorrhea and pos-
teriorly causes postnasal drip. This hyperresponsiveness can be due
to structural or functional components of the nasal mucosa altered
through genetic or pathologic factors. The exact mechanisms of
nonallergic rhinitis conditions are poorly understood because of
their multiple presentations.
Infectious Rhinitis/Rhinosinusitis
Acute sinusitis (rhinosinusitis) most commonly occurs as a compli-
cation of viral upper-respiratory infections (URIs). Viral URIs
cause nasal mucosal edema, which leads to obstruction of the sinus
openings and ciliary impairment. Bacteria proliferate in the stag-
nant mucus as well as the low–oxygen-tension environment of
the sinus cavities. Chronic rhinosinusitis is the result of long-term
obstruction and/or dysfunction of the sinuses. Chronic inflamma-
tion leads to chronic low-grade infections.
Prevention
Environmental control of allergens can improve the severity of aller-
gic rhinitis and can reduce the need for medications. Environmental
control should be thorough if treatment is sought, but the full ben-
eficial effects of the change may take weeks to months. Mild disease
can usually be managed with avoidance measures. Complete avoid-
ance of allergen, particularly pollen, is usually not feasible.
Reduction of dust mite allergen exposure can be done in the fol-
lowing ways: remove carpets and soft toys, use covers impermeable
to allergen for mattresses and pillows, vacuum beds weekly, and
wash bedding at 60 degrees Celsius (140 degrees Fahrenheit). Pet
dander avoidance can only be effectively managed by removing
the pet and carefully cleaning all carpets, furniture and mattresses.
Clinical Manifestations
If the patient presents with symptoms of palatal itching, nasal itch-
ing, ocular symptoms, or sneezing, consideration should be given
to an allergic cause.
The presentation of nonallergic rhinitis is dependent on the type
of nonallergic rhinitis. Overall, patients with nonallergic rhinitis
lack other allergic conditions.
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The vasomotor rhinitis patient will present with predominantly
nasal obstruction and rhinorrhea. Typically, symptoms are trig-
gered by temperature, exercise, and environmental stimuli (odors,
smoke, and dust).
NARES patients generally have more intense symptoms than
vasomotor rhinitis or allergic disease patients. NARES patients
present with paroxysms of flares to include sneezing, watery rhi-
norrhea, nasal itching, congestion, and some anosmia. NARES
patients have eosinophils on a nasal smear, but lack other allergic
evidence by skin-prick testing.
Gustatory rhinitis sufferers complain of nasal congestion and
rhinorrhea associated with ingestion of foods and, sometimes,
alcoholic beverages.
Nasal crusting, dryness, and fetor are the characteristics of atro-
phic rhinitis. These findings are due to glandular cell atrophy.
Patients will have abnormally wide nasal cavities and may have
squamous metaplasia.
Occupational rhinitis patients have components of allergic and
nonallergic disease. Patients present with nasal congestion and rhi-
norrhea triggered by an occupational exposure. Symptoms are pre-
sent during duty and generally improve away from the work
environment. Substances leading to symptoms include irritating
chemicals, grain dust, ozone, lab animal antigens, and wood. Often
occupational rhinitis co-exists with occupational asthma.
Hormonal rhinitis manifests as nasal congestion during preg-
nancy or the menstrual cycle. Pregnant women are six times more
likely to have rhinitis and sinusitis than nonpregnant women. Rhi-
nitis usually resolves two weeks postdelivery.
Drug-induced rhinitis occurs with certain medications. ACE
inhibitors, phosphodiesterase-5 selective inhibitors, alpha-receptor
antagonists, and phentolamine are common triggers. Patients pre-
sent with rhinorrhea and nasal congestion.
Rhinitis medicamentosa is a condition that presents with severe
congestion. It is caused by prolonged and repetitive use of topical
nasal decongestants. It can also be associated with cocaine use.
Anatomic rhinitis is more likely in patients who present with uni-
lateral nasal symptoms.
Rhinitis
Infectious rhinitis presents with sinus tenderness, erythema to the
mucosa, postnasal drainage and sometimes periorbital edema.
Diagnosis
The diagnosis of allergic rhinitis, nonallergic rhinitis, and infectious
rhinitis is based largely on history and physical examination. Other 55
diagnostic testing can be performed to aid in providing a more
definitive diagnosis or to rule out other causes.
Allergic rhinitis is confirmed by IgE reactivity to environmental
allergen sensitivity through skin-prick testing. When skin-prick
testing is difficult to interpret or if it is not feasible, serum–aller-
gen-specific IgE testing can be used. Nasal smears looking for
eosinophils are not recommended for routine use in the diagnosis
of allergic rhinitis.
Other testing available for evaluation of rhinitis includes nasal
endoscopy, rhinomanometry, and radiologic imaging. Fiberoptic
nasal endoscopy is reserved for those with atypical symptoms or
an inadequate response to treatment. Rhinomanometry measures
airflow obstruction in the upper airway. Rhinomanometry pro-
vides an objective measurement of nasal congestion. Rhinomano-
metry is used to evaluate clinical response to interventions and
assess anatomic severity, such as in patients with obstructive sleep
apnea. Radiologic imaging, such as computerized tomography
(CT) and magnetic resonance imaging (MRI), is used to evaluate
anatomic structure. Imaging may not correlate well with nasal
function and is expensive.
If a provider suspects a cerebrospinal fluid (CSF) leak, the rhi-
norrhea can be evaluated for beta transferrin protein, which is pre-
sent only in CSF.
History
The best diagnostic tool in the evaluation of rhinitis is the history.
Information regarding previous evaluation and treatment should
be elicited. A positive family history of rhinitis points towards
 allergic disease. The history of symptoms should include questions
regarding congestion; sneezing; rhinorrhea; sore throat; dry throat;
cough; itchy, red, or tearing eyes; voice changes; sinus symptoms of
drainage; pressure or pain; snoring; ear pain or loss of hearing; and
smelling difficulty.
When gathering the details of each symptom, evaluate the onset
(such as those in childhood), frequency (episodic versus continual),
pattern (seasonality), characteristics of secretions, triggers, severity
(to include quality of life evaluation), and associated geographic
location or environment (home versus work). Once a trigger is
identified, history needs to be gathered even further to evaluate
the possibility of modifying the exposure.
Physical Examination
As with any disease process, the physical examination provides
clues into the diagnosis. Although the physical examination in rhi-
nitis patients should focus on the nasal mucosa, other body areas
should be examined to rule out other processes. For example, the
tympanic membranes should be examined for mobility, retraction,
erythema, and Eustachian tube dysfunction.
Examination of the eyes in allergic rhinitis might show that the
conjunctiva have edema, erythema, and/or cobblestoning. Exces-
sive lacrimation could be another finding. Darkening of the skin
of the lower eyelids is prevalent in allergic disease and is also called
1 Symptomatic Care Pending Diagnosis
“allergic shiners.”
Allergic and nonallergic nasal mucosa may have a similar
appearance. The nasal mucosa may appear boggy with a bluish
appearance or be erythematous. Excessive watery-clear mucus
might be present. Turbinate hypertrophy is another physical exam-
ination finding in rhinitis. Other nasal mucosa findings to look for
are nasal polyps, sinusitis, septal deviation, septal perforation, and
crusting.
Looking for elongated facies, mouth breathing, and a high arch
in the palate may provide a clue to the severity of the nasal obstruc-
tion. The tonsils and adenoids should be examined for enlarge-
ment. Posterior nasal drainage and cobblestoning in the
oropharynx are common findings in rhinitis patients.
The skin examination provides useful information in the patient
with rhinitis. Atopic dermatitis or urticaria may be findings asso-
ciated with allergic disease. The skin should be evaluated for der-
matographism. Patients with dermatographism cannot be
evaluated for allergic disease using skin-prick testing.
56
Differential Diagnosis
Many different pathologic conditions can present similarly to rhi-
nitis. Conditions to keep in mind while evaluating and treating a
patient for rhinitis include: nasal polyps, ciliary dyskinesia syn-
drome, anatomic abnormalities such as deviated septum or tumors,
nasal turbinate hypertrophy, cerebrospinal fluid rhinorrhea, phar-
yngonasal reflux, systemic disorders such as Wegener’s disease,
aspirin intolerance, and other medication side effects.
Treatment
Overall
Current guidelines in treatment of rhinitis do not take cost into con-
sideration. However, the individual treatment goals should be
based on factors such as age, route of administration preference
(i.e., nasal versus oral), severity, seasonality, side effects, cost, ben-
efit to comorbid conditions, and onset of action. For example,
onset of action is an important consideration for an individual
who has more episodic symptoms. Also, individual patients
respond differently to treatment regimens within a given group.
Avoidance
Due to the lack of high-quality evidence, implementation of avoid-
ance measures is largely based on panel recommendations. In addi-
tion, the ubiquitous nature of allergens may limit the effectiveness
of the avoidance measures. For dust mites, encasing pillows
and bedding in dust mite resistant materials may be beneficial.
Pollen is seasonal and can be minimized by keeping the windows
closed, using air conditioning, and limiting outdoor exposure.
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Using particulate filters in the home can also assist in reducing
overall allergen load of pollens and dust. Avoiding basements
and lowering household humidity may reduce the amount of mold
exposure patients receive. Pet avoidance can only be reached by
ridding the house of the pet altogether. Other, less-effective mea-
sures include limiting exposure of the pet to the house and/or
bedroom.
Intranasal Corticosteroid (INS)
Intranasal corticosteroids are first-line treatment for moderate to
severe allergic rhinitis and most nonallergic rhinitis conditions.
All allergic rhinitis symptoms can be treated with INS. The intra-
nasal corticosteroids budesonide aerosol (Rhinocort Aqua), fluti-
casone propionate aqueous (Flonase), and beclomethasone
aqueous (Beconase AQ) preparations all have a Federal Drug
Administration (FDA) treatment indication of nonallergic rhinitis.
Intranasal corticosteroid side effects include irritation, bleeding,
and perforation of the nasal septum; rarely, local candidiasis is
seen with INS use. They are safe to use in pregnancy. No single
INS preparation is more efficacious than, or has any relevant dif-
ference from, any other. INS has negligible hypothalamic-pitui-
tary-adrenal axis suppression, and systemic burden is clinically
insignificant.
Intranasal Anticholinergic (IP)
Ipratropium bromide (Atrovent), a specific intranasal anticholiner-
gic, inhibits parasympathetic function in the nasal mucosa. The
parasympathetic blockade reduces the output of secretions from
seromucus glands in the nose. Ipratropium can be used in treatment
of anterior watery rhinorrhea but has a very limited role in reduc-
ing postnasal drip, nasal congestion, or sneezing. Topical ipratro-
pium prior to ingestion of food can be used as pretreatment of
gustatory rhinitis and is effective in treatment of the common cold
and skier’s nose. Side effects of IP include nasal dryness, burning,
irritation, stuffy nose, headache, and dry mouth.
Intranasal Antihistamine (INA)
Azelastine (Astelin) is a nasal spray approved by the FDA for aller-
gic and vasomotor rhinitis. Olopatadine (Patanase) intranasal
spray has been approved for seasonal allergic rhinitis. INA has fas-
ter onset of action than intranasal corticosteroids. INA should be
taken twice per day for maximum clinical benefit and may benefit
those with nasal congestion. INA does not produce a significant
amount of sedation, but side effects include headache, epistaxis,
bitter taste, and nasal irritation.
Nasal Cromolyn
Cromolyn (NasalCrom) should be considered for early mild rhini-
tis, but should not be considered a first-line treatment in allergic
rhinitis. Nasal cromolyn can be used prior to allergen exposure
for prophylaxis of episodic allergic rhinitis. Cromolyn is mostly
void of side effects. Cromolyn inhibits mast cell degranulation
and is administered three to four times a day. Cromolyn has very
limited usefulness for nonallergic rhinitis conditions.
Nasal Saline
Using nasal saline to irrigate the nasal cavities may remove mucus,
enhance ciliary movement, improve sinus opening, and remove
allergic and irritant particles. Several devices exist including: the
neti pot, a nasally adapted plastic bottle, and a pulse irrigator. Evi-
dence suggests that hypertonic saline provides modest benefit over
isotonic saline, although it might be more irritating.
Topical Decongestants
Topical decongestants reduce congestion, but have no effect on
itching, sneezing, or rhinorrhea. Oxymetazoline (Afrin), a common
topical decongestant, causes nasal vasoconstriction. Vasoconstric-
tion can cause tissue hypoxemia and inflammation, leading to
severe rebound nasal congestion. Topical decongestants are not
recommended for continued use because they can cause rhinitis
medicamentosa.
Oral Antihistamines
Oral antihistamines block H1 receptors, thereby reducing nasal
and palatal itching, rhinorrhea, sneezing, conjunctivitis, and urti-
caria. Nasal congestion is not treated well with oral antihistamines.
First-generation oral antihistamines are poorly selective for H1
receptors. The sedative effects of these antihistamines result from
crossing the blood–brain barrier; they have been linked to indus-
trial accidents and contribute to loss of function at work and
school. For these reasons, first-generation antihistamines have lim-
ited usefulness. Second generation H1 antagonists have excellent
evidence for therapeutic efficacy. These medications may have
some role in the treatment of nonallergic rhinitis because of their
anticholinergic properties, but consideration must be given to these
systemic properties, including dry mucous membranes, blurry
vision, constipation, tachycardia, and urinary retention. A combi-
nation of intranasal corticosteroid treatment with oral antihista-
mines may be effective for sneezing and rhinorrhea in NARES.
Leukotriene Receptor Antagonists (LTRA)
Leukotriene receptor antagonists were originally studied in the
treatment of asthma. The only LTRA approved by the FDA for
treatment of allergic rhinitis is montelukast (Singulair). Montelu-
kast is clinically efficacious in both perennial and seasonal allergic
rhinitis. Montelukast is approved for children 6 months and older
and has a pregnancy category B rating. The oral antihistamine lor-
atadine (Claritin) and montelukast have similar efficacy, and can
have additional benefit when used together. Although rare, monte-
lukast has been associated with adverse psychiatric behavior,
including suicidality. LTRA have no role in nonallergic rhinitis.
Oral Decongestants
Oral decongestants such as pseudoephedrine reduce nasal conges-
tion. Oral decongestants have a sales restriction in many states.
Side effects include insomnia, anorexia, irritability, and palpita-
tions. Blood pressure elevation is rarely a concern in controlled
hypertensive patients or in normotensive patients. Oral deconges-
tants should be considered last-line treatment for nonallergic rhini-
tis conditions.
Systemic Corticosteroids
Few studies are available to support the use of systemic steroids in
the treatment of rhinitis. Oral corticosteroids may have a role for
severe resistive rhinitis, but not as first-line treatment. Short-term
use of 5 to 7 days of oral corticosteroids is the standard, but they
should not be used for longer than 3 weeks because of the risk for
adverse effects. Oral steroids should be used as first-line treatment
for severe nasal polyposis, a subset of anatomic rhinitis. Systemic
steroids should not be used in children or pregnant women. Intra-
turbinate injections of corticosteroids have no role in the treatment
of rhinitis. Parenteral corticosteroids are contraindicated because
of long-term effects.
Surgery
Surgery can reduce nasal obstruction caused by septal deviation,
turbinate hypertrophy, or adenoid hypertrophy. Procedures that
can be performed include nasal polypectomy, septoplasty, reduc-
tive hypertrophic turbinate surgery, adenoidectomy, and endo-
scopic sinus surgery. Two nerves can be transected to decrease
the parasympathetic nerve supply to the nasal mucosa: the vidian
nerve, through endoscopic resection; and the anterior ethmoid
nerve, through electrocoagulation, which leads to reduced nasal
secretions.
Anti IgE
Omalizumab (Xolair) is a monoclonal antibody available for the
treatment of poorly controlled asthma, but it might have a role
in the treatment of allergic rhinitis.1 Omalizumab binds to IgE, hin-
dering its relationship with inflammatory cells. Omalizumab only
1
Not FDA approved for this indication.
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binds to circulating IgE and not bound IgE. Due to its high cost,
reports of anaphylaxis, and its injectable only formulation, omali-
zumab has a limited role in allergic rhinitis treatment.
Immunotherapy
Allergen extract immunotherapy has been used in the treatment of
respiratory allergic disease since 1911, and its efficacy has been
documented since the 1970s. The amount of allergen in each immu-
notherapy dose is slowly increased with each dose until a mainte-
nance phase is reached. Immunotherapy is an effective treatment
for allergic rhinitis and is the only treatment proven to alter the
course of allergic disease. Debate exists regarding which form of
immunotherapy is superior. Contraindications to immunotherapy
include beta-blocker use, due to complications in treating anaphy-
laxis, and uncontrolled underlying diseases, such as uncontrolled
asthma.
Subcutaneous immunotherapy uses the injectable form of aller-
gen extract. Adequate treatment usually consists of a 3- to 5-year
course of immunotherapy. Subcutaneous immunotherapy is indi-
cated in those patients for whom medications and avoidance mea-
sures are inadequate, as well as those with only a few relevant
allergens. The inherent risk of subcutaneous immunotherapy is sys-
temic anaphylaxis, therefore it is dosed in the physician’s office.
The rate of local reactions in subcutaneous immunotherapy is
0.6-58% and systemic reactions is 0.06 to 0.9%. The risk of death
is 1 per 2.5 million injections. Subcutaneous immunotherapy is
covered by most insurance plans.
Studies for local-route immunotherapy (noninjected), many of
which were carried out in Europe, have only been undertaken in
adults. Local routes of immunotherapy include sublingual, local
nasal, oral, and bronchial. Indications for local-route immunother-
apy are the same as those for subcutaneous immunotherapy.
Sublingual immunotherapy was approved by the FDA in April
2014. Sublingual immunotherapy formulations in the United
States are low dose compared to those used in Europe, but have
limited allergens available. The risk profile is low and therefore
can be dosed at home. The rate of local reactions with sublingual
Rhinitis
immunotherapy is 0.2-97% and systemic reactions is 0.056%. No
deaths have been reported with sublingual immunotherapy use.
Some medical allergy providers use subcutaneous extracts (aque-
ous) as sublingual therapy, but this is an off-label use.
Use of local nasal immunotherapy is used mostly in Europe. Oral
and bronchial immunotherapy are not supported by evidence. 57
Monitoring
The provider should consider stepping down treatment when the
patients’ symptoms have been controlled. The Total Nasal Symp-
toms Score [TNSS] is a subjective assessment of the patient’s spe-
cific symptoms, including rhinorrhea, nasal congestion, sneezing,
and pruritus, and can be used to assess effectiveness of medications.
The Rhinoconjunctivitis Quality of Life Questionnaire can also be
used. Consideration for referral to an allergist might be extended to
patients who have had a prolonged course, secondary infections,
polyps, or other comorbid conditions including chronic sinusitis
and asthma, or if immunotherapy is a consideration.
Complications
Rhinitis is associated with multiple complications including
fatigue, decline in cognitive function, loss of productivity, head-
ache, and disturbance of sleep. Patients with mild disease may
experience these in mild form. Patients with moderate to severe dis-
ease may experience these complications in addition to impairment
of activities, leisure, and work or school functioning.
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Surg Clin North Am 20:61–71, 2012.
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approved treatment method in the United States? Curr Allergy Asthma Rep
11:4–6, 2011.