Allergic Rhinitis

Allergic Rhinitis (AR) is an inflammatory disorder of nasal mucosa marked by nasal

congestion, rhinorrhea, and itching, often accompanied by sneezing and congjungtival
inflammation. Its recognition as a major chronic respiratory disease of children rests largery
on its high prevalence, detrimental effects on quality of life and school performance, and
comorbidities. Children with AR often have related conjunctivitis, sinusitis, otitis media,
serous otitis, hypertrophic tonsils and adenoids, and eczema. Childhood AR is associated
with a 3-fold increase in risk for asthma at an older age. Over the past 50 yr an upsurge in AR
has been observed throughout the word, particularly in areas where its prevalence previously
had been low. In prosperous societies, 20-40% of children suffer from AR. The symptoms
may appear in infancy; with the diagnosis generally established by the time the child reaches
age 6 yr. The prevalence peaks late in childhood.

Risk factors include family history of atopy and serum immunoglobulin (Ig) E higher
than 100 IU/mL before age 6 yr. Early life exposure and/or their absence have a profound
influence on the development of the allergic phenotype. The risk increases in children whose
mothers smoke heavily, even before delivery and especially before the infants are 1 yr old,
and those with heavy exposure to indoor allergens. A critical period exists early in infancy
when the genetically susceptible individual is at greatest risk of sensitization. Delivery by
cesarean section is associated with AR and atopy in children with a parenteral history of
asthma or allergies. This association may be explained by the lack of exposure to maternal
vaginal/fecal flora during delivery. Children between 2 and 3 yr old who have elevated
anticockroach and antomouse IgE are at increased risk of wheezing, AR, and atopic
dermatitis. The occurence of 3 or more episodes of rhinorrhea in the first year of life is
associated with AR at age 7 yr. Intriguingly the exposure to dogs, cats, and endotoxin early in
childhood protects againt the development of atopy. Prolonged breastfeeding is beneficial,
but it does not need to be exclusive there is also a decreased risk of asthma, AR, and atopic
sensitization with early introduction to wheat, rye, oats, barley, fish and eggs.

Etiology and classification

Two factors necessary for expression of AR are sensitivity to an allergen and the
presence of the allergen in the enviroment. AR classification as seasonal or parenteral is
giving way to the designations intermittent and persistent. The 2 sts of terms are based onn
different supposition, but inhalant allergens are the main cause of all forms of AR
irrespective of terminology. AR may also be categorized as mild-intermittent, moderate-
severe intermittent, mild-persistent, and moderated severe persistent. The symptoms of
intermitten AR occur on <4 days per week or <4 consecutive weeks. In persistent AR
symptoms occur on > 4 days per week and/or for >4 consecutive weeks. The symptoms are
considered mild when they are not troublesome, the sleep is noemal, there is no impairment
in daily activities, and no incapacity at work or school. Severe symptoms result in sleep
disturbance, and impairment in daily activities and school.
 In temperate climate, airbone pollen responsible for exacerbation of intermittent AR
appear in distinct phase: trees pollinate in the spring, grasses in the early summer, and weeds
in the late summer. In temperate climates, mold spores persist outdoors only in the summer,
but in warm climates throughout the year. Symptoms of intermittent AR typically cease with
the appearance of frost. Knowledge ef the time of occurrence of symyoms, of the regional
patterns of pollination and mold sporulation, and of the patient’s spescific IgE is necessary
for the recognition of the cause of intermittent AR. Persistent AR is most often associated
with the indoor allergens: house dust mite, animal danders, mice, and cockroaches. Cat and
dog allergies are major importance in the united states. The allergies are of major importance
may remain airbone for a prolonged time. The ubiquitous major cat allergen, fel d 1, may be
carried on cat owners’ clothing into such “cat free” settings as schools and hospitals.

Intermittent symptoms Persistent symptoms

- <4 days/week - ≥4 days a week

- or <4 weeks at a time - and/or ≥ 4 week at a time

Mild Moderate-to-severe
One or more items
- Normal sleep
- Normal daily activities - Abnormal sleep
- Normal work and school - Impairment of daily
- No troublesome symptoms activities, sport and leisure
- difficulties caused at
school or work
- troublesome symptoms

Figure 143-1 Aria classification of allergic rhinitis. Every box can be subclasiified further
into seasonal or parennial on the basis of timing of symptoms or when causative and allergen
therapeutic factors are considered. For example, a UK patient with grass pollen allergy might
have moderate-to-severe persistent seasonal rhinitis in june and july and be suitable for
specific allergen immunitherapy.

PATHOGENESIS

The exposure of an atopic host to an allergen lead to spesific IgE production. The clinical
reaction on reexposure to the allergen have been designated as early-phase and late-phase
allergic responses. Bridging of the IgE molecules on the surface of mast cells by allergen
initiates early-phase allergic response, characterized by degranulation of mast cells and
release of preformed and newly generated inflammatory mediators including histamine,
prostaglandin 2, and the cysteinyl leukotrienes. Late-phase allergic response appears 4-8 hr
following allergen exposure. Inflammatory cells, including basophils, eosinophils,
neutrophils, mast cells, and mononuclear cells, infiltrate the nasal mucosa. Eosinophils
release proinflammatory mediators. Including cysteinyl leukotrienes, cationic proteins,
eosinophil peroxidase and major basic protein, and serve as a source of interleukin (IL)-3, IL-
5, granulocyte-macrophage colony-stimulating factor, and IL-13, repeated intranasal
introduction of allergens cause “priming”-a more brisk response even with a lasser
provocation. Over the course of an allergy season a multifold increase in submucosal mast
cells takes place. These cells, once thought to have a role exclusively in the earlyphase
allergic response, have an important function in sustaining chronic allergic disease. Allergen,
autoantigens, and components of superimposed infectious agents activate the immune system.

Clinical manifestations

Symtoms of AR may be ignored or mistakenly attributed to a respiratory infection. Older

children blow their noses, but younger children tend to sniff and snort. Nasal itching brings
on grimacing, twitching, and picking of the nose that may result in epistaxis. Children with
Aroften perform the allergic salute, an upward rubbing of the nose with an open palm or
extended index finger. This maneuver reliever itching and briefly unblocks the nasal airway.
It also gives rise to the nasal crease, a horizontal skin fold over the bridge of the nose. The
diagnosis of AR is based on symptoms in the absence of an upper respiratory tract infection
and structural abdomalities. Typical complaints include intermittent nasal congestion, itching,
clear rhinotthea, and conjunctival irritation. Symptoms increase with greater exposure to the
responsible allergen. The patients may lose their sense of smell and taste. Some experience
headaches, wheezing, and coughing. Nasal congestion is often more severe at night, causing
mouth breathing and snoring, interfering with sleep, and arousing irritability.

Signs on physical exam include abnormalities of facial development, dental malocclusion,

and the “ allergic gape” or continuous open mouth breathing, chapped lips, “allergic shiners”
(dark circles under the eyes), and the transverse nasal crease. Conjunctival edema, itching,
tearing, and hyperemia are frequent findings. A nasal exam performed with a source of light
and a speculum may reveal clear nasal secretions ; edematous, boggy, and bluish mucus
membranes with little or no erythema; and swollen turbinates that may block the nasal
airway. It may be necessary to use a topical decongestant to perform an adequate
examination. Thick, purulent nasal secretions indicate the presenceof infection.

Differential diagnosis
Evalution of AR calls for a thorough history, including details of the patient’s enviroment and
diet and family history of allergic conditions such as eczema, asthma, and AR, physical
examination, and laboratory evaluation. The history and laboratory findings provide clues to
the provoking factors. Symptoms that include sneezing, rhinorrhea, nasal itching, and
congestion and the laboratory findings of elevated IgE, specific IgE antibodies, and positive
allergy skin test results typify AR. Intermittent AR differs from persistent AR by history and
skin test results, nonallergic rhinitides cause sporadic symptoms. Their causes are often
unknown. Nonallergic inflammatory rhinitis with eosinophil imitates AR in presentation and
response to treatment, but without elevated IgE antibodies. Vasomotor rhinitis is
characterized by excessive responsiveness of the nasal mucosa to mucosa to physical stimuli.
Other nonallergic conditions, such as infectious rhinitis; structural problems, including nasal
polyps and septal deviation; rhinitis medicamentosa (caused by the overuse of topical
vasoconstrictors) ; hormonal rhinitis associated with pregnancy or hypothyroidism;
neoplasms; vasculitides; and granulomatous disorders may mimic AR. Occupational risks for
rhinitis include exposure to allergens (grain dust, insects, latex, enzymes) and irritants (wood
dust, paint, solvent, smoke, cold air).

Table 143-1 Causes of nonallergic rhinitis

Structural/mechanical factors
Deviated septum/septal wall anomalies
Hypertrophic turbinates
Adenoidal hypertrophy
Foreign bodies
Nasal tumors
Benign
Malignant
Choanal atresia
Infectious
Acute
Chronic
Inflammatory/immunologic
Granulomatosis with polyangiitis
Sarcoidosis
Midline granuloma
Sistemic lupus erythematosus
Sjogren syndrom
Nasal polyposis
Physiologic
Ciliary dyskinesia syndrome
Atrophic rhinitis
Hormonally induced
Hypothyroidism
pregnancy