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30 Chronic Cough inChildren: Upper Respiratory Tract Related Etiologies
reason for the indication of endoscopic sinus surgery. If outpatient treatment is not
possible and severe sinusitis occurs, extensive examination and lengthy surgical dissection may be considered as a way to effectively drain the nasal cavities [15,
18, 28].
397
30.4 Gastroesophageal Reflux
andLaryngopharyngeal Reflux
Gastroesophageal reux is a physiological occurrence observed in around 40–65%
of infants [29]. The occurrence of reux often reaches its highest point between the
ages of 1 and 4 months, and it tends to subside naturally by the time the child
reaches 12months of age [30]. Although reux is a common phenomenon in infants,
it becomes pathologic GERD when accompanied by additional symptoms such as
recurrent regurgitation, dystonic neck posturing and back arching, cough, apnea,
bradycardia episodes, and/or failure to thrive. In such cases, further investigation
and intervention are necessary [31].
The challenge of establishing a connection between cough and GERD in children mostly stems from the complexities associated in diagnosing GERD.The etiology of cough is predicated upon the stimulation of vagal nerve bers located within
the esophagus, which triggers the cough reex. Vagal stimulation subsequently elicits a parasympathetic response, resulting in the manifestation of cough and/or bronchospasm [32].
In more severe cases of GERD, passage of reuxed uid into the larynx may
result in microaspiration followed by tracheobronchitis and pneumonia. In addition,
GERD can cause persistent cough even in the absence of esophagitis, that is, in the
form of laryngopharyngeal reux [33].
The identication of GERD and laryngopharyngeal reux can be established by
a comprehensive assessment of the patient’s medical history and a thorough physical examination. Nevertheless, further diagnostic testing is necessary for individuals
experiencing complications related to GERD.The diagnostic procedures that can be
employed include barium contrast and uoroscopic imaging of the upper gastrointestinal tract, pH meter analysis, esophageal manometry, endoscopic biopsies, and
scintigraphy. Nevertheless, current recommendations do not endorse the routine utilization of these investigations for the diagnosis of GERD, except if there is a suspicion of anatomical irregularity or the presence of particular warning symptoms
[31, 33].
In the management of GERD, patients are typically advised to adhere to certain
dietary recommendations. These recommendations involve avoiding the consumption of a high-fat diet and, if applicable, making efforts to reduce excess body
weight. Additionally, it is recommended to refrain from eating before 2h of sleep
and to abstain from consuming substances such as caffeine, carbonated beverages,
alcohol, and citrus goods. It is advisable to request patients to abstain from smoking
and raise the head of the bed. Proton pump inhibitors have traditionally served as the
primary empirical therapy for coughs associated with GERD [34]. In the context of
398
nonacidic reux, drugs that function by creating a protective layer or physical barrier to prevent reux could be used as an additional or perhaps alternative therapy
approach. The etiology of GERD has been associated with gastroesophageal dysmotility, which involves anomalies in delayed gastric emptying as well as diminished pressure or improper temporary relaxation of the lower esophageal sphincter.
A number of prokinetic medicines have the ability to enhance gastrointestinal motility, making them potentially valuable additions to antireux treatment [35, 36]. The
utilization of surgical interventions plays a signicant role in the treatment of
patients who do not respond well to conventional treatments [35].
T. Ramasli Gursoy and L. Gochicoa-Rangel
30.5 Otogenic Cough
The phenomenon known as the ear-cough reex was initially documented by Arnold
in the year 1832, and subsequently recorded by Itard in 1842. The prevalence of this
condition ranges from 1.7% to 4.2% [37]. The nerve known as Arnold’s nerve originates from the jugular ganglion of the vagus nerve, and it exits through the tympanomastoid ssure. Its typical function is providing innervation to the skin of the
posterior and inferior meatus. Nevertheless, the reex of ear-cough may be induced
with the stimulation of the anterior wall in approximately one-third of instances,
and it is observed bilaterally in approximately two-thirds of cases. The activation of
the Arnold’s nerve can also result in non-respiratory manifestations, including vomiting and syncope [37, 38]. The prevailing factors contributing to this phenomenon
typically involve the presence of foreign objects and impacted cerumen within the
ear canal. The diagnosis is frequently made incidentally when there are no accompanying ear symptoms, as the otoscope is not regularly employed during the evaluation of a patient presenting with a persistent cough [39].
30.6 Laryngeal Clefts
Laryngeal clefts are congenital anomalies that have a relatively low prevalence and
are distinguished by an atypical connection between the respiratory tract and the
digestive tract. Based on the Benjamin-Inglis categorization method, there exist four
distinct categories of laryngeal clefts [40]. Type 1 laryngeal cleft refers to a specic
anomaly characterized by a deciency in the interarytenoid mucosa or musculature,
which does not extend beyond the voice cords. Type 1 laryngeal cleft typically manifests as persistent cough, recurring episodes of pneumonia, and difculties with eating [41]. Type 1 laryngeal cleft has been found to have possible associations with
comorbidities such as laryngomalacia, trachea-esophageal stula, GERD, and diseases including Trisomy 21 [42]. The identication of type 1 laryngeal cleft might
provide challenges in the diagnostic process, mostly because of the diverse array of
non-specic symptoms exhibited by the affected individuals. The precise identication of a medical problem may experience a delay due to the potential for symptoms
to be mistakenly associated with alternative disorders, such as asthma, allergies, or
30 Chronic Cough inChildren: Upper Respiratory Tract Related Etiologies
399
GERD.Direct laryngoscopy is often regarded as the preferred diagnostic method for
identifying type 1 laryngeal cleft. The management of Type 1 laryngeal cleft can be
approached through conservative or surgical methods. The conservative approach to
treatment encompasses the feeding and swallowing therapy. The surgical intervention involves the administration of different drugs into the interarytenoid area or the
mending of the cleft using endoscopic suturing. The customization of management
choices should be based on the severity of the patient’s symptoms [43, 44].
30.7 Conclusion
The presence of a chronic cough is frequently observed in several illnesses, often
exhibiting overlapping characteristics that transcend the boundaries of multiple
medical specialties. The comprehensive evaluation of individuals experiencing persistent coughing necessitates a multidisciplinary strategy and effective collaboration among specialists in the elds of pulmonology, gastroenterology, and
otolaryngology. UACS, CRS, and GERD are prevalent causes of chronic nonproductive cough observed in pediatric medical settings. A considerable number of
these patients are not widely recognized for their challenging nature in terms of both
diagnosis and treatment. However, employing a methodical and comprehensive
approach within a multidisciplinary context has the potential to provide favorable
outcomes in diagnosing and treating the majority of patients.
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401
Upper Respiratory Tract Comorbidities
inChildren withWheezing
ŞuleBüyük Yaytokgil andErsoyCivelek
31.1 Introduction
Multimorbidity is a common problem in patients with chronic diseases such as
asthma/recurrent wheezing and may cause poor quality of life and management of
diseases, and increased health care utilizations [1, 2]. Multimorbidity is more common especially in patients with difculty treated and/or severe asthma [3]. Treating
the multimorbidities may minimize future asthma exacerbations [1] and improve
the asthma treatment.
Upper respiratory co-morbidities are common and important in diagnosis and
management of children with recurrent wheezing/asthma, because they may confuse with wheezing and cause unnecessary treatments, or they may sometimes contribute to poor disease control by aggravating symptoms [4]. Therefore, recognizing
and treating upper respiratory comorbidities in asthma/recurrent wheezing may
improve their outomes [4, 5].
This chapter is an overview of the prevalence, clinical features, diagnosis, and
management of the upper respiratory co-morbidities (chronic-rhinosinusitis, nasal
polyposis, allergic rhinitis, vocal cord dysfunction, and obstructive sleep apnea syndrome) in children with recurrent wheezing/asthma.
31
Ş. Büyük Yaytokgil
Department of Pediatrics, Division of Pediatric Allergy and Immunology, Ankara Research
and Training Hospital, Ankara, Turkey
E. Civelek (*)
Department of Pediatrics, Division of Pediatric Allergy and Immunology, Private Hospital
Memorial Ankara, Ankara, 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_31
403
404
Ş. Büyük Yaytokgil and E. Civelek
31.2 Pathogenesis oftheUpper andLower Respiratory
Diseases Comorbidities
Respiratory systems are divided into two sections: upper and lower. Diseases related
with both sections may affect each other [6] and was dened as a one way or united
way [7–10], because they share many anatomical and histological properties [6–8]
and some mechanisms were suggested [8–11] (Table31.1).
The rst mechanism is the protective function of nose for avoiding bronchoconstriction. The nose is the entrance of air and the place where the air warms, lters,
and humidies [10], but if the nose impaired, the bronchoconstriction may occur
[12]. Also, nasal breathing was reported as protected against the onset of exerciseinduced asthma, whereas oral breathing is more likely to exacerbate symptoms.
During the oral breathing, cold and dry air reach the lung directly and provocate
bronchoconstriction [13]. Therefore, in any nasal pathology, the nasal breathing is
interrupted and the nasal shielding function is cessated and consequently bronchial
disorders may be triggered [10].
The second suggested mechanism is the similarity in histology [8]. Both nose
and bronchi consist of a pseudostratied respiratory epithelium, and their mucosae
have ciliary epithelium on the basement membrane, lamina propria, glands, and
goblet cells under the basement membrane [11]. Epithelium is the rst defense
mechanisms for microorganisms; therefore, if any defect occurred in the epithelium, the barrier function could be lost, consequently microorganisms can penetrate the epithelium and then provocate inammation [11]. İmpairment of the
epithelium functioning is one of the contributive factors for the development of
airway diseases [6, 10].
Also, there are some common immunopathology in the inammation of the
upper and lower airways, because mast cells, T lymphocytes, and eosinophils might
inltrate both airways; and may cause the symptoms [9]. Inammation in the upper
respiratory mucosa with specic allergens or microorganisms may trigger inammation in the lower respiratory mucosa by drainage of inammatory mediators [6,
10, 14, 15]. This mechanism, which is called as postnasal drainages of the inam-
mation [6, 14], is the third mechanism.
The fourth mechanism is the inammation caused by the same triggers. One
study described allergic rhinitis (AR), rhinosinusitis, and asthma as “one way and
one disease” and indicated that same triggers cause inammation in both the nose
and the lungs [7]. These common triggers are allergens, pathogens, and environ-
Table 31.1 Possible
mechanisms for upper
respiratory comorbidities of
the patients with asthma/
wheezing
1. Function of nose
2. Similar epithelium and mucosal membrane
3. Postnasal drainages of the inammations
4. İnammation with similar agent (such as virus/bacteria/
antigen)
5. Type 2 inammation
6. Neural reex (similar innervation)
31 Upper Respiratory Tract Comorbidities inChildren withWheezing
mental factors. Previously, atopic march was considered to consist of two steps,
rst atopic dermatitis and then respiratory allergies, e.g., AR and asthma—as a
similar tract disease [7]. However, recently a study showed that there is no specic
or typical sequence of symptoms development that characterizes this atopic march,
indeed the classic sequence of eczema, wheeze, and rhinitis were relatively rare
(around 2–4%) by the nal time [16] and increased gradually from infancy to age
4–5years, with little change thereafter. On the other hand, some viruses affect both
upper and lower respiratory systems and they may cause rhinitis, sinusitis, bronchiolitis, and pneumonia. Tobacco smoke exposure is one of the common environmental factors which also affect both upper and lower respiratory tract [17]. Also,
some drugs such as aspirin and betablockers may trigger both asthma and AR
symptoms [7].
The fth mechanism is the Th2 type inammation which may cause chronic
airway diseases such as asthma, AR, and chronic sinusitis [6, 18]. Presence of the
Th2-type inammatory process dominated by eosinophils at one site of the airways
may cause to release cytokines (including IL-4, IL-5, IL-13) into the blood stream
which can stimulate the bone marrow and as a result of this can cause the increasing
of systemic eosinophilic inammation [6, 14]. Persistent type 2 inammation continuously damages the epithelium and cause to exacerbate the clinical symptoms
[18]. In patients with asthma, the coexistence of other type 2 inammatory diseases
produced greater decline in lung function and more symptoms [18].
“Neural reex” is another mechanism reported that may provide communication
between the nose and bronchi, because the nose and bronchi share the same adrenergic and vagal innervation [9, 19]. The nasobronchial reex, consists of broncho
constriction and increase in pulmonary resistance following the exposure of the
nose to cold air or irritants [19]. Also, it was previously reported that nasal challenges induced to the bronchoconstriction and also bronchial provocations can
cause the nasal reactions [14].
On the other hand, CST1 (cystatin SN gene) was detected to be higher in patients
with AR and asthma than patients with AR alone; therefore, CST1 may be a biomarker for airway allergic diseases [20].
All of these mechanisms show that inammation of the upper airway can lead to
abnormal changes in the mucosa of the lower airway [14, 20]. Knowing the similari-
ties and interactions of upper and lower airway may facilitate the managements of
the respiratory diseases with coexistence of each other.
405
31.3 Epidemiology ofUpper Respiratory Comorbidities
ofAsthma
Asthma is a chronic respiratory disease characterized with chronic airway inammation [1]. The main goal of asthma therapy is achieved to the minimal or no
symptoms of disease, normal sleep and activities, and optimal pulmonary function [1]. In order to achieve these goals, knowing and eliminating asthma comorbidities is important.
406
Ş. Büyük Yaytokgil and E. Civelek
Mirabellia etal., reported that 87.8% of the children with asthma had other comorbidities, whereas 65% of the children without asthma had comorbidities [5]. One
study reported that 21% of the patients with asthma have one to two coexisting conditions, 30% have three to four coexisting conditions, and 45% have more than ve
coexisting conditions [21]. Prevalence of comorbidities varies according to different
studies and countries [22]. The study on asthmatic children showed that respiratory
allergies were the most common detecting comorbidity (up to 30.5%) [5]. A recent
study reported that only 13% of the children with asthma did not have any comorbidity, while 37% of asthmatic children had respiratory comorbidities (rhinitis or sinusitis or snoring), and 40% had both respiratory and extra-respiratory comorbidities
[23]. AR were the most common respiratory comorbidities of asthma [22]. AR was
detected in 64% of the asthmatic patients, and asthma was detected in 20% of AR
patients. Also, 24% of the patients with chronic rhinosinusitis (CRS) was reported to
have asthma and 8% of the asthmatic patients have CRS [24]. Allergic sinusitis was
reported in 20% of the asthmatic children [22]. Global Initiative for Asthma (GINA)
advices to evaluate the nasal involvements in asthma patients [1].
Comorbidities increase the risk of exacerbations, rates of hospitalizations, visits
of emergency department (ED), and visits of unscheduled doctor ambulatory care
[25]. Healthcare expenditures and hospital readmissions are directly related to the
number of chronic conditions [21]. Previous studies reported that asthmatic children
with respiratory comorbidities had more exacerbations, and lower sleep quality
[23]. AR and sinusitis are associated with more severe symptoms, poorly controlled
asthma, more exacerbations, and more sleep disturbances [26]. The frequency of
asthma attack and emergency department visits were reported more in children with
comorbidities compared to those without comorbidities [5].
31.4 Risk Factors forMultimorbidity/Comorbidity inAsthma
Detecting the risk factors for comorbidities of asthma may facilitate the development of preventive strategies to decrease comorbidies and its cost. There have been
several studies that investigated the risk factors for developing comorbidities in
patients with asthma [18, 23, 27, 28].
The EuroPrevall-iFAAM birth cohort study reported that independent to IgE sensitization, coexistence of allergic comorbidities like rhinitis and eczema were
detected to be more frequent in asthmatic children than general population [27].
And Asthma comorbidities may occur as a result of both genetic and environmental
factors [20, 23]. But the presence of type 2 inammations may also increase the
coexistence with other chronic airway diseases such as chronic sinusitis, AR,
etc. [18].
Maternal history of asthma, breastfeeding, early mold exposure, and current
environmental tobacco smokes exposure were reported as the signicant risk factors
for asthma-respiratory comorbidities in children [23]. Higher body mass index
(BMI) was detected in asthmatic patients with respiratory comorbidities than asthmatic patients with extra-respiratory comorbidities [23]. Age may be another risk
31 Upper Respiratory Tract Comorbidities inChildren withWheezing
407
factor for asthma comorbidity, as the coexistence of CRS and asthma increased by
age was reported in a small study [28].
Presence of allergy in the family, cesarean, and early-age onset-symptoms were
reported as other risks for multimorbidity of allergic diseases including asthma, AR,
and eczema [27]. The risk of gender is conicted. In one study, female gender was
reported as a protective factor [27]. In contrast, female was associated with increased
risk of AR and sinusitis comorbidities in asthmatic patients [26]. But in another
study, gender was not determined as a risk factor for comorbidities [22]. While in
another study, comorbidities in asthmatic patients were more prevalent in males
before puberty, and in females after puberty [29].
Also, some countries or regions had more asthma comorbidities. For example,
nasal polyposis as comorbidities of asthma was less common in China compared to
Europe [30]. Maybe, because in Chinese patients, nasal polyposis was less related
to Th2-typed inammation [30].
Immunological diseases such as antibody deciency is one of the main contributors for inammation in both upper and lower airways [31], which may increase the
risk of asthma comorbidity. Some other comorbidities may increase the frequency
of upper respiratory comorbidities of asthma such as hypertrophy of tonsils and
adenoids [15, 32].
31.5 Upper Respiratory Comorbidities ofWheezing/Asthma
Upper respiratory comorbidities are common in patients with asthma and GINA recommend to evaluate for nasal involvements [1]. Some upper respiratory diseases
such as AR and CRS may be an important risk factor for new onset asthma [9].
Bronchial hyperactivity was detected in patients with AR without asthma, forced
expiratory ow at 25% and 75% (FEF 25–75) was suggested as an early marker of
bronchial involvement in patients with allergic rhinitis who had only nasal symptoms
[9]. Co-existence of upper respiratory comorbidities such as AR and sinusitis may
increase asthma symptoms [26]. Presence of upper respiratory comorbidities increase
the costs and outcomes of asthma, mimic or aggravate symptoms of asthma, decrease
both adherence or effectiveness of treatments, and decrease the quality of life [4].
The upper respiratory co-morbidities of wheezy children are vocal cord dysfunction,
obstructive sleep apnea syndrome (OSAS), CRS, nasal polyposis, and AR.
31.5.1 Vocal Cord Disfunction (VCD)
Vocal cord disfunction (VCD) is characterized with inappropriate movement of the
vocal cords and triggered by some factors such as exercise, psychological stress,
local irritation (reux) [33]. The prevalence of the VCD in the pediatric population
has not been adequately estimated [34] .VCD and asthma often coexisted with each
other [33]. In a retrospective study (n=292), Traister etal., reported that 32.6% of
VCD patients had concomitant asthma [35].