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34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
451
rhinitis, from mild to persistent and severe forms. Regarding otolaryngology, adenoid
hypertrophy, nasal septum deviation, turbinate hypertrophy, chronic sinusitis, nasal
foreign bodies, cystic brosis/ciliary dyskinesia, and nasal tumors should be considered in the differential diagnosis in the pediatric age group. Treatment options should
be determined individually according to the age and symptoms of the patients.
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M. C. Gökgöz et al.
Allergic Rhinitis: Pediatric Pulmonologist Perspective
AhmetTurkeli andBatuhanBerkDemir
35.1 Introduction
Lung diseases in children are a leading cause of morbidity and mortality worldwide.
Some of these include asthma, cystic brosis, neuromuscular disorders, pulmonary
hypertension, interstitial and diffuse lung diseases, sleep disorders, aerodigestive
disorders, opportunistic and complicated pneumonia, apnea, acute and chronic
respiratory failure, primary ciliary dyskinesia, and undiagnosed genetic childhood
respiratory diseases.
Allergic rhinitis (AR) is a chronic inammatory disease of the nasal mucosa
induced by environmental allergen exposure and the immunoglobulin E (IgE)
response [1, 2]. AR can be intermittent or persistent, based on the duration of symptoms, and mild, moderate, or severe, based on the severity of symptoms [3].
Environmental factors that induce AR are pollen, dust mites, mold fungi, and animal
dander [4]. Typical symptoms include nasal discharge, sneezing, nasal irritation,
and nasal congestion [2]. Also observed are extranasal symptoms including watery
eyes, redness, swelling, irritation in the eyes, itching on the palate, and itching in the
ears [2, 3]. The underlying inammatory process and/or dysfunction of the nasal
mucosa [3] are responsible for these symptoms. AR can also negatively inuence
patients’ quality of life, cause sleep disturbances, and result in poor work or school
performance [3, 5].
35
A. Turkeli (*)
Division of Pediatric Immunology and Allergy, Department of Pediatrics, Kutahya Health
Science University Medical Faculty, Kutahya, Turkey
B. B. Demir
Department of Pediatrics, Kutahya Health Science University Medical Faculty,
Kutahya, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_35
455
456
A. Turkeli and B. B. Demir
Common in pediatric patients, allergic rhinitis can have signicant consequences
for respiratory functions. A pediatric pulmonologist must assess the effects of allergic rhinitis on the respiratory system and overall respiratory health.
35.2 Allergic Rhinitis andAsthma
The airway consists of a unied structure that extends from the nostril to the small
peripheral airways [6]. Unied airway disease (UAD) refers the common epidemiological and pathophysiological relationship among chronic inammatory diseases
of the upper and lower respiratory tracts, including AR, chronic rhinosinusitis
(CRS), and asthma [7–9].
Asthma is a chronic inammatory disease of the airways characterized by structural changes and the involvement of numerous cells and cellular components,
including mast cells, eosinophils, T cells, macrophages, and epithelial cells. Asthma
patients exhibit wheezing, sputum production, varying degrees of ventilation limitation, and airway hypersensitivity to environmental bronchospasmogenic stimuli [10].
At the beginning of the 1990s, asthma and rhinitis were viewed as separate maladies associated with IgE sensitivity. In the European Community Respiratory Health
Survey (ECRHS), rhinitis was recognized as an independent risk factor for asthma
in both allergic and non-allergic patients [11].
Upper and lower airways are interconnected anatomically, histologically, and
immunologically, forming a unied airway system in which inammation in one
part of the airways effects the other [7]. Numerous studies conducted in accordance
with the “one airway, one disease” theory have shown that the comorbidity of rhinitis and asthma conveys a single disease pattern in the airways. AR and asthma share
the same etiological factors, inammatory cell prole, location in the respiratory
system, and treatment similarities [12]. Various international guidelines, including
Allergic Rhinitis and Its Impact on Asthma (ARIA), the International Consensus
Statement on Allergy and Rhinology: Allergic Rhinosinusitis and Rhinosinusitis,
and the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS), investigate the interaction between the upper and lower airways [7].
35.2.1 Epidemiological Relationship
Reportedly, the prevalence of AR ranges from 5 to 50% worldwide [4]. According
to studies, the prevalence of AR in children may be higher than in adults, with 80%
of patients experiencing symptoms before the age of 20, and in some countries, 40%
of patients developing symptoms before the age of 6 [13]. In patients with rhinitis,
the risk of developing asthma is three times higher than in those without rhinitis,
regardless of the presence of atopy [8, 14]. There is substantial evidence that AR in
childhood or adolescence is a risk factor for subsequent asthma development [10,
15, 16]. 80–90% of asthma patients have rhinitis, and 20–40% of rhinitis patients
have asthma [14, 17].
35 Allergic Rhinitis: Pediatric Pulmonologist Perspective
457
Untreated or inadequately treated rhinitis can triple the risk of asthma attacks,
and bronchial hyperreactivity is common among rhinitis patients [12]. It has been
shown that infants with increased airway sensitivity to histamine are four times
more likely to develop asthma [18]. In non-asthmatic but symptomatic patients with
AR, the methacholine bronchial provocation test revealed high rates of positivity
[19, 20].
The coexistence of AR and asthma poses a signicant risk for deterioration in
asthma control and asthma exacerbations [6]. Those who suffer from both rhinitis
and asthma tend to have more severe conditions [14, 15]. Large population-based
studies have demonstrated a correlation between the two diseases’ severity [10, 14].
In children with asthma and AR, more frequent visits to the emergency room and
admissions indicate inferior disease control, more frequent exacerbations, and
increased hospitalizations. This circumstance results in increased healthcare utilization and asthma costs among asthmatic children with AR [8, 21]. In a study of
approximately 30,000 asthmatic patients conducted in Japan, it was discovered that
patients with concomitant AR were more likely to have uncontrolled asthma as
dened by the GINA guidelines than patients without AR [22]. In contrast, Ponte
and colleagues [23] demonstrated that moderate to severe rhinitis is associated with
inadequately controlled asthma.
Allergens are potent inducers of AR and asthma. Indoor allergens, such as house
dust mites, are linked to asthma, whereas outdoor allergens, such as pollen, are
more often linked to AR [24].
35.2.2 Relationship Between theUpper andLower Respiratory
Tracts fromaPathophysiological Standpoint
The passageway that runs from the nose and paranasal sinuses to the bronchi is
deemed a functional unit according to the unied airway model [10, 14]. Chronic
inammation is observed in the nasal mucosa and bronchial mucosa, the two most
signicant regions of this unied airway. While the nasal and bronchial mucosa
share similar characteristics, such as pseudostratied epithelium and the presence of
both ciliated and columnar cells on the basement membrane, they exhibit signicant
differences at the submucosal level. In contrast to the nasal mucosa, which is dominated by vascular structures, the bronchial airways are dominated by muscle structures encircling the airways [7, 25]. Vasodilation and edema result from inammation
of the nasal mucosa, whereas inammation of the bronchial mucosa causes smooth
muscle contraction [14].
Although there is mounting evidence that AR may inuence the clinical course
of asthma, the mechanisms connecting upper and lower airway dysfunction remain
poorly understood. Various hypotheses, including both direct and indirect effects,
have been proposed to explain the pathophysiological connection between the upper
and lower respiratory tracts, specically, an altered respiratory pattern, pulmonary
aspiration of nasal contents, the nasal-bronchial reex, and the uptake of inammatory mediators into the systemic circulation [7, 20].
458
A. Turkeli and B. B. Demir
Due to its anatomical location, the nostril warms, lters, and moistens the air that
is inhaled. In fact, exercise-induced bronchospasm is caused by the chilling and drying of the airways caused by forced mouth breathing during vigorous exercise. In
addition, numerous submucosal glands in the nostril are capable of sterilizing the air
via the release of antibacterial enzymes. Since nasal congestion in AR forces the
patient to breathe through the mouth, nasal function may be completely or partially
impaired. Mouth breathing allows allergens and frigid air to enter the bronchial
airways directly, causing hypersensitivity in the airways [7, 26, 27].
35.2.3 Effects Systemic ofNasal Inflammation ontheLower
Respiratory System
Regardless of the tissue in which the allergic reaction occurs, it triggers not only a
local immune response but also a systemic response by allowing the inammatory
reaction to spread to other organs via the circulatory system. Even in the absence of
clinical asthma, patients with AR exhibit not only a local inammatory response
effecting the nasal airway, but also a more widespread inammation in the airways
[14]. In patients with seasonal AR but without asthma, for instance, nasal allergen
tests not only induce bronchial airway sensitization but also increase eosinophil
counts in sputum samples [28]. When segmental bronchial provocation is performed
on AR patients without asthma, it induces nasal inammation and an increase in
peripheral blood eosinophils [29]. It has been shown that eosinophilic inammation
occurs in the nasal mucosa of asthmatics in response to bronchial allergen provocation [26]. This occurs in the bronchial mucosa of patients with allergic rhinitis. The
release of eosinophils, basophils, and their progenitor cells from the bone marrow
[7] is likely caused by the absorption of inammatory mediators (e.g., IL-5 and
eotaxin) from sites of inammation into the systemic circulation. Before and 24h
after nasal allergen testing, bronchial and nasal biopsies were performed on AR
patients, and an increase in the number of eosinophils was observed in the nasal and
bronchial epithelium at the end of 24h [30].
The nasobronchial reex is another mechanism that may explain bronchial
hyperreactivity in AR patients. Bronchoconstriction is mediated by vagal, trigeminal, and afferent receptor pathways. Nose, trachea, pharynx, and respiratory tract
contain receptors that are sensitive to mechanical and chemical variables. The neural signals then travel to the central nervous system and activate the efferent vagus
nerve, resulting in hyperreactivity of the bronchial smooth muscle. Exposure of the
nasal mucosa to cold and dry air, for instance, may induce sudden bronchoconstriction in asthmatic patients [6, 15, 31].
Impaired Mucosal Function: It has been demonstrated that allergic inammation of the respiratory mucosa disrupts the barrier function of the epithelium. This
disruption in epithelial integrity may result in increased allergen absorption and IgE
synthesis, affecting the lower respiratory tract as a consequence. Alternately,
impaired nasal mucosa may be more susceptible to viruses, resulting in an increase
in allergic susceptibility and an increase in asthma incidence [25, 32].
35 Allergic Rhinitis: Pediatric Pulmonologist Perspective
459
35.2.4 Immunopathology
Recent research has demonstrated that the immunological mechanisms underlying AR and atopic asthma are identical. Both the upper and lower respiratory
tract tissues contain structural (epithelial cells, mast cells, and dendritic cells)
and inltrative (eosinophils, Th2 cells) cell types. In allergic airway diseases,
airway inammation is characterized by Th2 cells (Th2 cells, type 2 B cells,
IL-4-producing natural killer T cells (NKT cells), basophils, eosinophils, mast
cells, ILC2, IL4, IL5, IL13, IL-25, IL-31, and IL-33). In addition to the adaptive
immune response, the upper and lower respiratory tracts share similarities with
the innate immune system, such as epithelial barrier function and innate immune
cells (ILCs) [7, 9, 33]. Airway epithelial cells swiftly secrete the cytokines IL-25,
IL-33, and thymic stromal lymphopoietin (TSLP) when exposed to environmental antigens, viruses, and allergens. These so-called alarmins directly activate
ILC2s, which produce the prototypical type 2 cytokines IL-5 and IL-13 [7]. It is
common to observe nasal inammation in asthma patients without rhinitis symptoms and bronchial inammation in rhinitis patients without asthma symptoms.
Even in individuals with no history of bronchial hyperreactivity, nasal allergen
provocation can swiftly induce signicant pulmonary allergic inammation and
impaired respiratory function in patients with AR.In addition, segmental bronchial provocation may result in nasal symptoms and inammation in patients
with AR [34].
35.2.5 Effect ofRhinitis Therapy onAsthma
The most efcacious pharmacotherapy agent for AR is intranasal corticosteroids
(INC). They have powerful effects on symptoms, nasal physiology, and inammation of the upper airway mucosa. In a case-control study in which patients
with both AR and asthma were treated with INC, it was found that those patients
had signicantly reduced risks of asthma-related emergency department visits
and hospitalization [35]. Compared to placebo, a meta-analysis revealed that
INC improved PFT, BHR, asthma symptom scores, asthma quality-of-life scores,
and rescue medication use in patients who were not receiving adequate asthma
treatment. When INC was administered to asthmatic patients receiving inhaled
corticosteroids, no signicant change in asthma outcomes was observed [36].
These studies demonstrate the signicance of recognizing the connection
between rhinitis and asthma, both in terms of reducing somatic symptoms and
healthcare costs.
Contradictory effects of antihistamine medications on asthma. It is unclear
whether the benecial effects of antihistamines in asthma are due to direct effects
on the physiology of the lower airways or to the alleviation of rhinitis. Antihistamines
are not included in the management of asthma according to the 2022 Global
Initiative for Asthma guidelines, but it is crucial to remember that asthma treatment
is not “one size ts all” [37].
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A. Turkeli and B. B. Demir
35.2.6 Diagnostic andTherapeutic Strategies
Patients with rhinitis and/or asthma should undergo a thorough examination and
evaluation of both the upper and lower respiratory tracts [10, 27]. Symptoms,
including itching, sneezing, nasal discharge, nasal obstruction, and odor, are the
primary basis for a clinical suspicion of AR.These symptoms begin within minutes
of allergen exposure and last for approximately 2h. Late symptoms include nasal
congestion, loss of scent, hyperreactivity of the nose, and postnasal mucus discharge
[27]. Other associated symptoms (such as snoring, poor sleep quality, and ear congestion), shortness of breath with exercise, protracted cough after viral infections,
and nocturnal coughs should also be investigated and taken into account when
selecting a treatment [10, 38]. Evaluation of the clinical history should include an
investigation of the impact of rhinitis on daily life, school performance, and sleep,
as well as a comprehensive family history of allergic or immunological diseases [38].
A physical examination should also include anthropometric measurements and evaluation of the skin, ear, nose, oral cavity, and neck, with special attention devoted to signs
of atopy [10, 39]. Dennie Morgan lines (is a fold or line in the skin below the lower
eyelid), nasal bridging, allergic salute, conjunctivitis, and allergic shiner are typical
atopy symptoms [10, 27]. An essential overview is provided by anterior rhinoscopy, or
at least nasal examination, which can be performed with an otoscope. Secretions (typically aqueous in AR, change in color in non-allergic rhinitis (NAR), or infectious rhinitis), crusts, foreign bodies, septum deviation, septum perforation, polyps, and mucosal
edema are frequently observed. The use of nasal endoscopy is not required [10, 27].
In children and adolescents, allergic rhinitis is the most prevalent form of chronic
rhinitis; chronic non-allergic rhinitis, or CRS, is less common [40].
To diagnose A. rhinitis and asthma, allergy skin tests (SPT) or invitro measurements of specic IgE using the inhalant allergen panel are required. The SPT is the
primary invivo test recommended by international guidelines and is considered the
most sensitive and specic test for identifying atopy [41]. This information is
essential for distinguishing allergic rhinitis from non-allergic disease or other diseases such as CRS and devising an appropriate environmental control program.
Imaging is not required, but CT scanning of the nasal sinuses is recommended
when sinusitis is suspected [27].
35.2.7 Non-pharmaceutical Treatment Method
It has been demonstrated that avoiding the allergen to which a person is sensitive
can help control rhinitis and asthma in IgE-mediated sensitized individuals. All
patients with atopy should do this. Within 3months, the desired clinical improvement will be observed. Therefore, the effectiveness of non-pharmacological treatments is directly proportional to the duration of allergen exposure [10, 12].