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Ş. Büyük Yaytokgil and E. Civelek
Dyspnea, wheezing, stridor, chest pain or tightness, and throat discomfort are the
most common symptoms of VCD, and they may occur both at rest and during exercised [34, 36]. Cough and wheezing are also the most important symptoms of asthma,
so extensive differential diagnosis is necessary [37]. Short-acting beta-2 agonists
(SABA) are not enough to control the symptoms of VCD and intermittent inspiratory
symptoms occur [33]; therefore, these are important clues for differentiation of VCD
from asthma. There are some other differences between characteristics of asthma and
VCD.Such as the respiratory phases of symptoms; VCD occurs during inspiratory
phases [34]. Also, the duration time of onset of symptoms during exercises may be
different [38]. Exertional dyspnea occurs and peaks during exercise in patients with
VCD, whereas it usually peaks 5–20min after the end of exercise in patients with
asthma. But if both of them coexist in the same patient, time overlap can be seen [38].
31.5.2 Obstructive Sleep Apnea Syndrome (OSAS)
OSAS was seen in 1–3% of children [15], but in asthmatic children, the prevalence of
OSAS rises to 35–66% [39, 40]. A study reported that 47.3% of subjects with asthma
alone and 55.9% of patients with asthma and AR had OSAS [41]. Several studies
reported that OSAS and asthma were both confusing and contributed factors for each
other [15, 32, 39, 40]. There were many bidirectional connections between OSAS and
asthma, including incidence, risk factors, pathophysiology, and treatment [15, 32, 40].
A randomized sample survey of 1234 children aged 6–14 years in Belgium
revealed a two fold increase in OSAS symptoms among children with wheezing
[42]. Also, coexistence of OSAS was more frequently detected in children with
uncontrolled/poorly controlled asthma than in those with controlled asthma [32,
39]. Asthma and OSAS bidirectionally increase the severity of each other [40], also,
they shared multiple etiological risk factors [32], such as hypertrophy of tonsils,
adenoids, and obesity [15]. The prevalence of OSAS was higher in asthmatic children with AR than asthmatic children without AR [32]. Prevalence of attention decit hyperactivity disease was higher in asthmatic children with OSA than without
OSAS [32, 41]. OSAS was reported as an independent risk factor for uncontrolled
asthma in children [39]. Therefore, screening for OSAS should be performed routinely in all patients with severe, poorly controlled asthma [4]. Treating of OSAS
can ameliorate the severity of asthma [15]. So, the coexisting of OSAS should be
screened in patients with poorly controlled and/or severe asthma [4].
31.5.3 Allergic or Non-Allergic Rhinitis
Mucosal membranes irritations and inammations of nose is dened as rhinitis [1].
According to the presence of allergic sensitizations, rhinitis may be classied as
allergic or non-allergic rhinitis [1].
AR might promote, trigger, maintain, and worsen the asthma by several pathophysiologic mechanisms, such as the vagal reex (rhinobronchial reex), the continuous passage of allergic inammation from the nose to bronchi, the systemic
31 Upper Respiratory Tract Comorbidities inChildren withWheezing
409
release of mediators and cytokines, the irritant mechanism sustained by the postnasal drip, and the oral respiration caused by nasal obstruction, which promotes bronchial hyperreactivity (BHR) as dry and cold air penetrates into the bronchi [9].
AR frequently coexist with asthmatic patients [26], even most common comorbidities of asthma [22]. AR frequently occurs before the development of asthma in
children [11]. Also, AR may increase the risk of developing asthma [9]. AR may
cause worsening of asthma. Asthmatic patients with a combination of lower baseline lung function and allergic rhinitis (this indicates that more severe asthma) were
reported that more affected from the presence of AR [26].
Prevalences: AR is one of the most common comorbidities of asthma. Estimated
prevalence of AR is 10–40% in pediatric populations [43]. Most patients with
asthma, either allergic or non-allergic, have concurrent rhinitis. It is considered that
10.5–43% of patients with AR have asthma, and 40–90% of patients with asthma
have rhinitis [11, 12, 37, 44]. Also, 76.2% of the children with asthma, had AR [45].
Settipane etal. reported that the risk of asthma in patients with AR are more at 3
times compared with those without AR [46]. Also, another study indicated that AR
patients have eight-fold more risk of having asthma compared to patients without
AR [9]. And underdiagnosis of AR in patients with asthma was more common [12].
According to Allergic Rhinitis and its Impact on Asthma (ARIA), especially
patients with severe persistent rhinitis are prone to having asthma comorbidities
[47]. AR comorbidities in children with asthma can cause more hospitalization and
ED visits or underdiagnosed of asthma and associated with higher cost than children with asthma alone [44, 48]. In contrast to this, asthmatic participants with AR
had similar exacerbation rates compared to those without AR in both the Safety of
Inactivated Inuenza Vaccine in Asthma in Adults and Children (SIIVA) and Low
Dose Theophylline as Add-on Treatment in Asthma (LODO) cohorts [26]. Ohta
etal. reported that asthma control was signicantly worse in patients with a physician’s diagnosis of rhinitis by comparison with those without rhinitis [44].
On the other hand, some physicians indicate that AR may be an early stage of the
asthma [49]. Bronchial hyperactivity without clinical symptoms of asthma were detected
in most of the patients with AR, this may predict the future development of asthma [9].
Also, Leukotriene receptor antagonists (LTRAs) may reduce the inammation of
both the nasal and bronchial mucosae, thereby improving the total symptoms score
of both AR and asthma symptoms [10]. In real-life, in case of rhinitis and asthma
multimorbidity, which are also affected by environmental exposures, it is recommended to give digitalize and person-focused integrated treatments [50].
Immunotherapy also decreases the risk of asthma development [51] and can reduce
both nasal and bronchial symptoms [10].
31.5.4 Chronic Rhinosinusitis andNasal Polyposis
İnammation of nasal and paranasal sinus mucosae is called sinusitis and/or rhinosinusitis. According to durations of symptoms and inammations, rhinosinusitis is
classied as acute or chronic. Persistence of the symptoms of acute rhinosinusitis
for greater than 3 months despite standard medical management, including
410
Ş. Büyük Yaytokgil and E. Civelek
antibiotics, steroids, saline nasal rinses, and nasal sprays is diagnosed as chronic
rhinosinusitis (CRS) in children. And CRS is classied according to phenotypes
with nasal polyposis (NP) and without nasal polyposis [52, 53].
CRS is one of the most frequent upper respiratory tract comorbidities of asthma
[10] and associated with increasing risk of asthma exacerbations [3]. According to
clinical evidences, CRS affects both occurrence and course of the asthma [6]. Also,
CRS was dened as one of the markers of the severe asthma [4]. There were various
inammatory mechanisms dened, which affect the phenotypes of CRS [54]. For
example, the nasal polyp phenotype with high IL-5 was detected as strongly increased
the asthma prevalence [54]. Also, they reported that inammatory phenotypes might
have been an importance for comorbid asthma development [54]. In LODO cohort,
sinüsitis was associated with increasing exacerbations in asthmatic patients [26].
Presence of the AR and/or CRS was associated with poorer asthma control, more
exacerbations and ED visits and more difculty in controlling the symptoms [55].
Patients with asthma with NP showed greater decline in post-bronchodilator forced
expiratory volume in the rst second (FEV1) per year [56].
In United states, CRS was diagnosed approximately in 2% of children per year
[53]. CRS is associated with asthma, the prevalence of asthma was 5–12% in the
general population and 4% in pediatric population; whereas it goes up to 25% in
patients with CRS [57–59]. Tosca etal. reported rhinosinusitis in 44% of 128 asthmatic children evaluated by nasal endoscopy [60]. In another study, which investigated the CRS patients according to cluster analysis, the rate of asthma comorbidity
was ranging from 7% to 71% between the CRS cluster [54]. And another study
reported that 68% of the patients with asthma revealed sinus diseases which were
detected by sinus computer tomography (CT). Also, they detected several mucosal
thickenings which was associated with higher eosinophil levels in blood and sputum. And they reported that patients with more severe sinus disease showed a statistical trend toward lower values of mean FEV1 than others [61].
NP are benign edematous masses in the nasal cavities, paranasal cavities, or
both. Nasal obstruction, rhinorrhea, postnasal drip, and loss of smell are the main
symptoms of NP.And the estimated prevalence of NP is approximately 2–4% [62,
63]. The presence of NP with CRS was strongly correlated with asthma comorbidity
[54]. NP were diagnosed in 7% of asthma patients, and it were more frequently seen
in non-atopic asthma and late-onset asthma [6]. CRS frequently coexists with more
severe asthma, especially with NP [28, 54, 62, 63]. Due to the close relations
between RS and asthma, especially children and adolescents with poorly controlled
asthma should be investigated for occult or manifest RS [6].
As a result of the remodeling of nasal and paranasal sinuses mucosa, NP may
ocur [58]. Presence of NP affects the severity of asthma; asthma was more severe in
CRS with NP (CRSwNP) than CRS without nasal polyps. But CRSwNP was associated with the late-onset, non-atopic severe asthma phenotype, so age was important for the occurence of nasal polyps [64]. Intolerance to aspirin (ASA) may also
be seen in patients with CRS and may provoke asthma and rhinitis symptoms; and
this was called “Non-steroidal anti-inammatory drugs exacerbated respiratory disease” (NERD) [4].
31 Upper Respiratory Tract Comorbidities inChildren withWheezing
411
CRS with type 2 (Th2) endotypes are more resistant to therapies compared to
CRS with type 1 and 3 endotypes [58]. But biological agents are available now and
they target type 2 inammation [47]. In the very near future, personalized medicine,
which is based on molecular biomarkers for the endotype or subendotype activated
in an individual patient, may be used for CRS patients [58].
Nasal congestion, impaired drainage of mucus at the ostiomeatal complex, stagnation of secretions, decreased ventilation, mucosal inammation, and decreased
mucociliary transport; all of them facilitate bacterial infection [62]. Also, inammatory discharge is dripped in to the lower airways from the nasal sinuses [11]. So,
European guideline suggests that antral irrigation should be considered in addition
to an adenoidectomy in children with severe asthma [57].
In asthmatic patients, endoscopic sinus surgery has been reported to improve
multiple clinical asthma parameters with improved overall asthma control, reduced
frequency of asthma attacks, and number of hospitalizations, as well as decreased
use of oral and inhaled corticosteroids [57]. Endoscopic sinus surgery is recommended especially in older children with CRS and especially in case of failure to
adenoidectomy [58].
Endoscopic sinus surgery for CRS can reduce the yearly incidence of new asthma
diagnoses; those patients whose surgery is late may develop higher rates of asthma
than those whose surgery is at an earlier timepoint [57].
After treatments of CRS, 79% of the poorly controlled asthmatic patients put off
bronchodilator therapy and 67% of them respiratory functional tests got back to
normal range [65].
Local or systemic corticosteroids, functional endoscopic sinus surgery can be
used for NP.And the presence of nasal polyps in severe asthma may help with the
choice of the biological therapy [1]. Because anti-IgE therapy improves both the
nasal polyps scores and asthma scores compared to basal scores [66]. Also, omalizumab improved the severity of symptoms and so quality of life scores in patients
with nasal polyps and comorbid asthma; the characteristics of these patients is being
under Th2 type inammations [66]. Treatment of CRS with nasal corticosteroids for
24weeks was reported to not improve the asthma control, in their placebo control
trial which investigated the effects of nasal mometasone on asthma outcome. So,
treating sinonasal diseases in asthma should be determined by the need to treat sinonasal disease rather than to improve asthma control [67].
31.6 Conclusion
Multimorbidity is common in patients with difcult treated and/or severe asthma
[3]. Especially, upper airway comorbidities are frequently coexistent with asthma as
a result of their similar patho-physiological mechanism, immunological predisposition, chronic airway mucosal inammation, and similar triggers [11]. Upper respiratory comorbidities are associated with poor symptoms control and increasing
exacerbations [4]. Also, these comorbidities increase rates of hospitalizations, visits
of ED, and visits of unscheduled doctor ambulatory care; so, this poses a signicant
412
Ş. Büyük Yaytokgil and E. Civelek
burden on individuals with asthma and the health care system. Therefore, diagnosis
and management of comorbidities are very important.
Both diagnosis and management of comorbidities should require multidisciplinary approach [4]. Because asthmatic children with multiple comorbidities are
taken care from different health providers, so their managements may have became
fragmented and less effective. In this perspective, comorbid disease may cause risk
for bad adherence to asthma treatment [31].
Allergic multimorbidities affect quality of life of both patients and families, so
treatments of asthma comorbidities may increase the quality of life [11]. Treating
the upper airway (nasal) disease reduce the bronchial hyperactivities and improve
the asthma symptoms [8]. Also, for decreasing the upper airway comorbidities,
early preventive strategies should be developed [18].
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415
Hemoptysis inChildren: ENT-Related
Etiologies
MugeOzcelikKorkmaz, CemalCingi, andKamilJaneczek
32.1 Introduction
Spitting up blood from the lungs or bronchial tubes due to pulmonary or bronchial
bleeding is known as hemoptysis. Based on the amount of blood lost, hemoptysis is
categorized as either non-massive or massive; however, there is no consensus on
what constitutes a “massive” hemoptysis. A daily blood loss of less than 200mL is
not considered substantial in this article. Both the pulmonary and bronchial arteries
supply blood to the lungs. Hemostasis from the bronchi, which is under systemic
pressure, is often more profuse than that from the lungs, which are under low pressure [1]. When making a diagnosis, the volume of blood loss is less helpful than
when it comes to guiding treatment [2].
Hemoptysis is the term used to describe the coughing up of blood from the lungs.
Hemoptysis can be mimicked by expectorating blood from the upper respiratory
system, nasopharynx, or upper digestive tract [3].
32
M. O. Korkmaz
Department of Otorhinolaryngology, Medar Hospital, Sakarya, Türkiye
C. Cingi (*)
Medical Faculty, Department of Otorhinolaryngology, Eskisehir Osmangazi University,
Eskisehir, Turkey
K. Janeczek
Department of Pulmonary Diseases and Children Rheumatology, Medical University of
Lublin, Lublin, Poland
e-mail: kamil.janeczek@umlub.pl
© 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_32
417
418
M. O. Korkmaz et al.
32.2 Severity ofHemoptysis
The severity of hemoptysis is not universally agreed upon. Although an estimate of
the amount of hemoptysis is helpful, other patient features and clinical judgment [4,
5] are more critical in determining the best course of treatment.
Hemoptysis will be classied according to the following scale (out of 6) for
this review:
• Scant: Less than 5mL (such as blood streaks) is considered “scant.”
• Mild to moderate: No signs of hemodynamic instability or compromised gas
exchange; mild to moderate (5–200mL within 24h).
• Massive: In the case of life-threatening or catastrophic bleeding, the amount lost
must be greater than around 200mL in less than 24h, and there must be signs of
hemodynamic instability (tachycardia, hypotension), aberrant gas exchange, dif-
culties keeping a patent airway, and highly rapid bleeding.
One of the most prevalent causes of hemoptysis in children is cystic brosis
(CF), and the volume estimates given above are based in part on a consensus guideline produced for individuals with CF [6]. There is no universal threshold for what
constitutes life-threatening or massive hemoptysis in adults. We use a threshold of
around 200mL, slightly lower than the threshold proposed by the CF consensus
guideline (240 mL). Massive hemoptysis in younger children lacks volume estimates. Regardless, these cutoffs are approximations at best and should be considered only one part of a comprehensive clinical evaluation. It is important to
remember that hemoptysis volume estimations are frequently inaccurate, do not
take patient size into account, and have a limited correlation with the source of
hemoptysis and clinical outcomes [3].
If feasible, rsthand observation of the bloody sputum and in-depth questioning
of the patient and caretakers is necessary to evaluate its volume and appearance.
Hemodynamic stability, estimated blood volume loss, and rate of bleeding are all
included in the global clinical evaluation to determine the severity (minimal, severe,
or fatal).
32.2.1 Non-massive Hemoptysis
Patient therapy for hemoptysis should focus on three main areas: stopping the bleeding, preventing aspiration, and treating the underlying cause. In the event of a medical emergency, the rst step is always to check the “ABCs” (airway, breathing, and
circulation) [2].
Acute, moderate hemoptysis due to bronchitis is the most prevalent presenting
symptom. It is possible to treat low-risk individuals with normal chest radiographs
as outpatients with strict supervision and suitable oral medications. An outpatient
assessment by a pulmonologist should be undertaken if hemoptysis continues or is
otherwise unexplained [2].