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M. Gümüşsoy and İ. Çukurova

22.9 Systemic Causes

22.9.1 Cystic Fibrosis
It is the most common autosomal recessive genetic disease in Caucasians. Water and salt transport in the cell membrane is disrupted, and there is a change in the composition of the uid secreted from the respiratory tract, pancreas, gastrointesti­nal tract, sweat glands, and other exocrine tissues. Because cystic brosis is a dis­ease that affects more than one system, it manifests itself with very different clinical signs and symptoms. Recurrent lung infections during childhood and adolescence, purulent sputum production, nasal congestion, nasal polyposis, chronic and persis­tent rhinosinusitis, asthma, clubbing of ngers, hemoptysis, biliary cirrhosis, meco­nium ileus, diabetes mellitus, delayed puberty, and infertility are among the ndings suggestive of cystic brosis. In addition to these clinical ndings, measuring 100mg of sweat chloride concentration above 60mEq/L in three separate periods conrms the diagnosis. Its treatment can be achieved with a multidisciplinary approach. Medical treatment (corticosteroids) and surgical treatment may be required in patients with polyps in the nasal cavity. The monitoring and treatment team should include a pulmonologist, gastroenterologist, metabolism and nutrition specialist, dietitian, physiotherapist, and microbiologist. Depending on the complications that arise, assistance from other branches is provided, thus prolonging the patients’ qual­ity and duration of life [5961].
22.9.2 Primary Ciliary Dyskinesia
It is characterized by chronic sinopulmonary infections starting from the neonatal period due to disorders in the structure and functions of cilia. It is characterized by ciliary immotility and ciliary dyskinesia. It is an autosomal recessive disease. There is a congenital disability in the structure and function of motile cilia. An increased incidence of infertility and situs in versus characterizes impairment in mucociliary ltration. Increased mucus and bacterial load in the airways is typical. While the diagnosis of cystic brosis can often be made at the age of one, in primary ciliary dyskinesia, if there is cardiac pathology, it may be delayed until the age of four or six if there is no [62].
For a denitive diagnosis, the nasal biopsy sample should be evaluated by video microscopy for cilia function and by electron microscopy for ultrastruc­tural cilia defect. The diagnosis must be conrmed by genetic evaluation. It is essential to have a history of recurrent respiratory tract infections, sinusitis and otitis attacks, cardiac pathology with bronchiectasis, or a history of a relative diagnosed with primary ciliary dyskinesia. In cases where nasal polyps are seen together with chronic rhinosinusitis in children, the most common differential diagnosis is cystic brosis and rarely direct rhinosinusitis. Ciliary dyskinesia should be considered [63].
ab
22 Nasal Congestion inChildren
305

22.10 Trauma/Iatrogenic Causes

22.10.1 Nasal Trauma-Septal Hematoma
Septal deformity in children is often seen after trauma and can occur anytime. The nose and mandible are the facial bones most frequently traumatized. During new­borns and childhood, fractures are not seen as often as in older children since most of the nasal skeleton has not developed and is cartilaginous. Therefore, nasal frac­tures are very rare in children under ve. Instead of fractures in the nasal bones, septal hematoma, abscess, or septum deviation are more common. Septal hematoma can be dened as bleeding between the mucoperichondrium, which vascularly sup­plies the septum cartilage, and the septal cartilage, and the separation of the muco­perichondrium from the septum. This condition blocks blood ow to the nasal septum and causes avascular cartilage necrosis. The collected blood and necrotic tissue become an excellent focus for infection of the nasal mucosa, and an abscess forms. Septal hematoma clinic manifests itself with nasal obstruction, and if not intervened, septal necrosis occurs, resulting in septal perforation and irreversible nasal deformities (Fig.22.5). Therefore, septal hematoma is a critical ENT emer­gency requiring early childhood diagnosis and treatment [64].
Examination of children after nasal trauma is more complex than for adults. Nasal palpation, deformity, and crepitation are problematic in pediatric patients. Endoscopic nasal examination is the gold standard. As an imaging modality, CT is the gold standard for imaging craniofacial and nasal fractures. Plain radiographs do not help diagnose nasal fractures in children. Signs and symptoms of septal hema­toma after nasal trauma may develop within 24–72h after the injury.
Fig. 22.5 (a) Septal hematoma anterior rhinoscopy nasal examination image, black star septal hematoma. (b) White arrow, septal hematoma image on paranasal coronal CT
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For this reason, if nasal congestion occurs after nasal trauma, it should be shared with the children’s families that it may be caused by septal hematoma. Septal hema­toma and abscess treatment is performed under general anesthesia with incision, drainage, and tampons placed in the nose. Antibiotics and nasal care should be rec­ommended to patients. The nasal tampon is usually left on for 2–3days. It may be difcult for children to tolerate tampons [65].
22.10.2 Septum Deviation
While some authors mention that birth trauma is an essential factor in forming sep­tum deviation in children, it has been reported that it can occur without birth trauma. As a result, septal deviation can cause nasal congestion in children and adults, whether congenital or acquired. The diagnosis of septum deviation can be easily made by endoscopic nasal examination. Its treatment is surgery, and its clinical indications must be based on solid foundations. These relate to the severity of the child’s nasal congestion, such as sleeping with an open mouth, sleep-disordered breathing, and craniofacial anomalies. Septoplasty is possible at any age but rarely performed before age seven. The reason is that septoplasty may negatively affect the development of the nose and face. This view stems from the fact that, anatomically, the story of the septal cartilage continues until the age of ve to six, and the vomer and perpendicular lamina continue until adolescence. On the other hand, waiting instead of surgically correcting a septum deviation that causes nasal congestion in a pediatric patient may be more harmful, considering the complications that may occur. Radiologically, paranasal CT is necessary for planning surgery [66, 67].
Surgically, to avoid disrupting the development of the nose and face, rearranging the septum with minimal resection of the cartilage part blocking the passage is a correct approach. In children, active growth foci should not be touched, and the bony septum should not be removed to avoid changes in facial development [68].
22.10.3 Nasal Foreign Bodies
Nasal foreign bodies are frequently encountered in children under the age of ve. The most important reason is that children in this age group put objects in their hands into their noses while crawling or playing on the ground. We can divide for­eign objects into two parts: living and non-living. Inanimate objects such as grains, beads, or buttons are more commonly seen in children. They often fall on the kitchen oor during cooking or are found by children at home [69].
When organic foreign bodies (chickpeas, beans, peas, etc.) come into contact with the nasal mucosa, they swell and become difcult to remove as they remain in the nose. Organic foreign bodies tend to swell and are generally more symptomatic than inorganic ones. For this reason, one should not wait for the removal of such foreign bodies and should be removed as soon as possible. Button batteries are attractive to children because of their small size and bright appearance; they are
22 Nasal Congestion inChildren
307
often inserted into the nose, ear, or mouth. Early diagnosis and urgent removal are essential. Any delay may lead to necrosis of the nasal mucosa and septal perfora­tion [70].
The most critical complaints of patients with foreign bodies in the nose are nasal congestion and foul-smelling nasal discharge. It may also cause symptoms such as nosebleeds, facial pain, nasal regurgitation, facial swelling, nasal crusting, and cough. Objects can be located in any nasal cavity region, inferior to the inferior turbinate or anterior to the middle turbinate. Sometimes, the foreign body is not vis­ible on nasal examination. When in doubt, the ideal method is rigid or exible nasal endoscopy (Fig.22.6). Edema, inammation, or bleeding around the foreign body may prevent the foreign body from being seen. Foreign body and unilateral choanal atresia, nasal tumor, nasal polyp, septal abscess, and septal hematoma should be considered in the differential diagnosis in pediatric patients presenting with unilat­eral nasal obstruction or foul-smelling, purulent nasal discharge. In diagnosing nasal and paranasal sinus foreign bodies, the most important diagnostic methods besides examination are plain radiographs, CT, and MRI [71].
In immobile patients with full cooperation, foreign bodies can usually be removed using appropriate tools without leaking into the nasopharynx, esophagus, or trachea. Organic foreign objects that do not have corners are round (balls, beads, etc.) or may break apart when held. They should be removed by going behind the thing and pulling it forward with a curved tool such as an Itard probe or an angled hook. No attempt should be made to grasp or remove round foreign objects from the front with a bayonet or forceps. Meanwhile, the foreign body may return to the
a b
a
b
Fig. 22.6 (a) The foreign body is in front of the middle turbinate during an endoscopic examina- tion of the left side of the nose. (b) The foreign body (plastic toy part) was removed from the nose
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nasopharynx, trachea, or esophagus. Suppose the foreign body is angular and prom­inent. In that case, it can be removed by grasping it with special tools such as bayo­net Hartman forceps, and if it is angular and small, alligator forceps. In cases where the nasal foreign body cannot be seen or retained, a balloon catheter can be applied [6971].

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Nasal Itching andSneezing inChildren
23
NurullahTüre andFatihOğhan

23.1 Introduction

Nasal itching and sneezing occur after neural activation stimulation by environmen­tal irritants and biological agents released during the local inammation process. In particular, sneezing protects the body by playing an essential role in protecting and clearing the airway from irritating substances. A runny nose, nasal itching, and nasal congestion often accompany sneezing. This condition is generally observed due to rhinitis seen in allergies and viral upper respiratory tract infections.
Rhinitis is inammation of the nasal mucosa. In rhinitis, nasal itching, sneezing, runny nose, and nasal congestion are observed. Along with rhinitis symptoms, accompanying complaints in the eyes, ears, and throat may be observed. Rhinitis is generally classied as allergic and non-allergic rhinitis [1, 2].
Regarding complaints, there is no signicant difference between allergic and non-allergic rhinitis. For this reason, most pediatric patients presenting with rhinitis complaints are diagnosed with allergic rhinitis. Treatment management is carried out according to this diagnosis. Sometimes, differential diagnosis can be difcult in pediatric patients due to overlapping conditions. It is difcult to determine its inci­dence epidemiologically due to the need for more data on the prevalence of nasal itching and sneezing in allergic and non-allergic rhinitis in pediatric patients.
This chapter explains the pathophysiology and etiology of nasal itching and sneezing in children, the differential diagnosis of co-occurring diseases, and appro­priate treatment options.
N. Türe · F. Oğhan (*) Kütahya Health Sciences University, Evliya Çelebi Training and Research Hospital, Izmir, Turkey e-mail: fatih.oghan@ksbu.edu.tr
© 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_23
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N. Türe and F. Oğhan

23.2 Pathophysiology

Itching is a nociceptive primitive defense mechanism that stimulates avoidance of inhaling harmful substances involving innate and adaptive immune mechanisms [3]. On the other hand, sneezing is caused by neural activation triggered by external environmental stimuli (irritants) or biological products formed in a local inamma­tory process. Sneezing is a central reex whose afferent arm begins in the nasal mucosa and whose efferent arm includes the nerves innervating the diaphragm, accessory respiratory muscles, and larynx. Sensory nerves in the nasal mucosa orig­inate from the ophthalmic and maxillary branches of the trigeminal nerve [4].
Terminal sensory nerve endings are mostly unmyelinated nociceptor C bers. Sometimes Aδ bers (Aβ bers) are also included [5, 6]. Nociceptor nerves respond to noxious external and internal stimuli through a series of receptors, such as tran­sient receptor potential vanilloid type 1 (TRPV1) and transient receptor potential ankyrin type 1 (TRPA1) [7].
Nasal nerve endings contain receptors for chemicals such as the Histamine 1 (H1) receptor or the cysteinyl leukotriene 1 receptor (CysLTR1) [8, 9].
While H1 receptors in nasal sensory nerve endings explain the sneezing that occurs during exposure to allergens, transient receptor channels explain the sneezing and itching that occur when exposed to non-antigenic irritating sub­stances [10].
Many pruritogens and receptors mediate itching, which occurs due to allergic rhinitis. After stimulation of nerve bers in the nasal mucosa and activation of mast cells, histamine is released, which causes nasal itching [11]. Histamine increased in the nasal lavage uid of allergic patients, but no increase was observed in non­allergic patients [12]. Neuropeptides such as substance P, CGRP, and vasoactive intestinal polypeptide (VIP) have been reported to be increased in the nasal lavage wash of patients with allergic rhinitis, which are thought to play a role in nasal itch­ing. Furthermore, nerve growth factor (NGF) is expressed in the nasal epithelium and peripheral nerves in the nasal mucosa, and the expression of this neuropeptide is signicantly increased after nasal allergen challenge in patients with allergic rhi­nitis compared to controls [13, 14]. House dust mites are affected by protease­activated receptor 2 (PAR2).
It has been shown to induce the release of inammatory cytokines and ultimately cause nasal itching [15]. Additionally, it has been reported that nasal itching increases when a TRPV1 activator such as capsaicin is administered to patients with allergic rhinitis during seasonal allergen exposure [16]. Nerve expression of TRPV1 is also increased in patients with non-allergic rhinitis [17]. This phenomenon sug­gests inammatory cytokines such as histamine and bradykinin cause nasal itching through TRPV1 receptors [18].
Physicians should know its close relationship with other allergic diseases, such as allergic conjunctivitis and asthma. Interestingly, pruritus has been reported as a preliminary symptom in patients with asthma [19]. Additionally, in a study investi­gating non-respiratory symptoms of acute asthma, nasal itching was observed before the asthma attack [20].