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294
M. Gümüşsoy and İ. Çukurova
the septum, through the cribriform plate, and extend to the skull base and even to the dura. They can be somewhere between the glabella and columella. Cystic expansion of the duct is dened as a dermoid cyst [17].
Nasal dermoid cysts may contain skin appendages (mesodermal). About 60% of the cysts are seen outside the nose, 30% are inside the nose, and the remaining 10% are of mixed type. Radiological examination is vital for diagnosis. CT is used for bone structures and relationships, and MRI with Gadolinium is used to evaluate intracranial extension and soft tissue. The treatment is surgical, and total excision is essential. Inadequate surgery may result in recurrence [18].
22.4.3.2 Nasal Glioma
Nasal gliomas are craniofacial masses developed from remnants of congenital benign neuro-glial tissues. Although they are perceived as tumors, they are accu­mulations of glial tissue in the extradural region. These are abnormal connections between the embryonic ectodermal and neuroectodermal parts due to the incom­plete closure of the anterior fontanelle between the nasal and frontal bones. About 30% of nasal gliomas are intranasal, and 15–20% have an intracranial connection with a brous band. On examination, it is smooth, not compressed by pressure; the overlying skin may be discolored or telangiectatic, and the mass is not attached to the mobile skin. Gliomas that have grown inside the nose can cause septal deviation. Sometimes, they can look like antrochoanal polyps. They may protrude from the anterior or posterior nasal cavity as pink-red polypoid masses. In MRI evaluation, detailed information about the intracranial distance can be obtained, and it also provides differentiation from other midline anomalies (encephalocele, dermoid cyst, etc.). Gliomas appear isointense on T1 and heterogeneous on T2 and do not capture contrast material. Treatment involves total excision of the mass [19, 20].
22.4.3.3 Encephalocele (Encephalo-Meningocele)
They are considered congenital neural tube defects. They always appear as extra­cranial herniation of meninges and brain tissue in the cranial defect area. They can be meninges (encephalocele), brain, and meninges (encephalo-meningocele). In nasal encephalocele formation, there is a bone defect between the frontal and ethmoid bones. The mass can be seen to grow with crying or with pressure on the jugular vein (Furstenberg test). Fronto-ethmoid encephaloceles are observed as compressible masses that give intranasal translucency. Clinically, they may pres­ent with nasal congestion, cerebrospinal uid rhinorrhea, or recurrent attacks of meningitis [21].
CT and MRI examinations are required for diagnosis. While CT is used to show the location of the bone defect at the skull base, MRI provides information about the sac content and intracranial extension (Fig.22.2). In cases where encephalocele is suspected, biopsy is not recommended due to intracranial relationship. When diag­nosed in the rst months of life, surgery should be planned to avoid the risk of meningitis and cosmetic deformity due to the growth of the mass. Treatment includes total removal of the group and repair of the dura [22, 23] (Fig.22.2).
22 Nasal Congestion inChildren
295
ab
Fig. 22.2 A 6-year-old girl complains of long-term nasal congestion and snoring. (a) Encephalocele extending to the inferior of the left frontal lobe with a brous band in the coronal MRI T1 section of the patient. (b) T2 section Coronal MRI imaging of the case
Differential Diagnosis
(a) Nasal glioma and dermoid cysts do not shrink upon examination, whereas
encephalocele is consistently soft and shrinks when pressed.
(b) Unlike nasal glioma and dermoid cysts, encephalocele may show
transillumination.
(c) The formation associated with cerebrospinal uid is encephalocele (herniation
of the meninges). (d) Nasal glioma has no connection with the intracranial region. (e) Encephalocele is pulsative (positive Furstenberg). (f) There is no pulsation in nasal glioma and dermoid cysts (negative Furstenberg). (g) Radiological imaging is sufcient for diagnosis. (h) Preoperative biopsy should not be performed. (i) While cranial bone defects are seen radiologically in encephalocele and der-
moid cysts, CT, and MRI, they are not seen in nasal glioma.
22.4.3.4 Nasolacrimal Duct Cyst (Dacryocystocele)
A nasolacrimal duct cyst develops due to incomplete canalization of the nasolacri­mal duct during fetal development and can cause signicant nasal obstruction in the newborn. Clinically, it is usually seen unilaterally, and the most common nding is epiphora. It is typical to see a bluish cystic lesion located in the medial canthus or an intranasal cystic mass [24].
Congestion in both noses occurs in 14% of cases and can close the nasal cavity and cause severe respiratory distress. CT is the method of choice for diagnosis. On CT, it can be seen as a cystic mass in the medial canthus region, expansion of the nasolacrimal duct, and a cystic mass lling the nasal passage at the level of the infe­rior turbinate. Its treatment is surgery [25].
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M. Gümüşsoy and İ. Çukurova

22.5 Infectious Causes

22.5.1 Rhinitis intheNeonatal Period
Since effective breathing for the newborn is only possible with an open nose, nasal congestion is vital, and severe hypoxia can have serious consequences. In the dif­ferential diagnosis, the most common cause of nasal congestion, apart from physi­ological and congenital causes, is rhinitis [46].
22.5.1.1 Rhinitis Etiology
1. Neonatal rhinitis.
2. Bacterial or viral rhinitis.
3. Iatrogenic rhinitis.
22.5.2 Neonatal Rhinitis
It is the most common cause of nasal congestion in the neonatal period. Regardless of the causative pathology, it is observed as runny nose and congestion in children under 3. Although its etiology is unknown, many causes have been blamed: viral, inammatory, vascular, drug-related, traumatic, hormones and drugs transmitted from the mother, etc. Nasal examination reveals bilateral nasal mucosa edema and mucoid nasal discharge. A regression in symptoms is observed after nasal lavage with physiological saline. Rhinitis symptoms resolve spontaneously over time [5, 26].
22.5.3 Bacterial or Viral Rhinitis
The causative agent is often bacteria such as maternal streptococci, staphylococci, chlamydia, gonorrhea, and syphilis, and less frequently, viral agents, especially respiratory syncytial virus. The clinical picture is nasal congestion after nasophar­yngitis and rhinitis [27, 28].
22.5.4 Iatrogenic Rhinitis
Iatrogenic rhinitis is due to secondary infection, trauma, nasal catheterization, or uncleaned residues such as meconium remaining in the nose. Another factor associ­ated with rhinitis ndings in the neonatal period is gastroesophageal reux. Nasal congestion causes an increase in negative intralaryngeal pressure during inspiration, thus facilitating reux. Therefore, in the presence of a persistent nasal obstruction in the neonatal period, the possibility of gastroesophageal reux should be investi­gated and treated [2729].
22 Nasal Congestion inChildren
297
22.5.5 Infectious Rhinitis (Rhinosinusitis)
Infectious rhinitis is often seen in childhood as inammation of the nose and sinuses due to viral, bacterial, and less fungal reasons. Acute upper respiratory tract infec­tions (rhinovirus) are infections of viral origin that are transmitted via droplets. Rhinitis clinically manifests with complaints of local itching and sneezing, conges­tion, and discharge (serous) in the nose, along with systemic symptoms such as chills, weakness, and fever. Flu (inuenza) has a more severe course than rhinovi­rus. It causes more serious damage to the upper respiratory tract, often leading to secondary infection. The incidence of sinusitis increases in children after rhinovirus or inuenza is the causative agent of rhinitis. Sinusitis is seen in 5–10% of children due to upper respiratory tract infections, especially between 6 and 8. It is more appropriate to call this condition, which clinically concerns both the nose and sinuses, rhinosinusitis rather than sinusitis [30, 31].
When we examine it physiopathologically, viral infections disrupt nasal muco­ciliary activity, cause mucosal edema, and narrow the sinus ostium, thus preparing the ground for the development of sinusitis. Due to the anatomical neighborhood of the sinuses with the nasal cavity, colonized Streptococcus pneumoniae, Haemophilus inuenzae, and Moraxella catarrhalis can pass into the sinuses. The mechanism can be summarized as ostium occlusion, negative sinus pressure, and infection. Impaired sinus circulation, mucus, and bacterial colonization in the sinus can easily result in acute bacterial rhinosinusitis. The most common viral agent that disrupts this defense mechanism is rhinoviruses. Rhinoviruses have a very high infection capac­ity [32].
Rhinosinusitis is more straightforward to develop in children in two ways. The rst reason is that the sinuses are small in volume, and their physiological defense mechanisms are not as fully developed as in adults due to their incomplete development.
Second, they experience frequent viral infections during childhood. The most critical risk factor for frequent infections is that the child goes to nursery or school. In the clinic of acute bacterial rhinosinusitis in children, nasal congestion, runny nose, posterior nasopharyngeal drainage, fever, cough, pain, especially on the side of the face where sinusitis occurs, edema, and halitosis (bad breath) are observed. ENT examination, especially nasal anterior rhinoscopy and endoscopic examina­tion, is vital for diagnosis. Nasal endoscopic examination is essential for evaluating many different structures, such as anatomical structures (septum deviation, turbi­nate hypertrophy), adenoid hypertrophy, and foreign bodies. Additionally, nasal endoscopy provides essential clues to show allergic rhinitis, nasal polyps, mucosal edema, scarring, discharge, and crusting within the nose [33].
In children under age 6, clinical ndings compatible with rhinosinusitis, history, and ENT examination are sufcient for diagnosis, and radiological evaluation is unnecessary. Radiological evaluation is useless, especially in children younger than 1year old. It cannot be evaluated because it is not radiologically developed except for the ethmoidal and maxillary sinuses. Ethmoid and maxillary sinuses are present
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at birth. The remaining sinuses begin to ventilate after age four and reach adult size by age twelve.
In summary, maxillary and ethmoid sinusitis may occur in the neonatal and infant period. The most frequently requested plain radiograph is the Waters radi­ography. However, its contribution is limited; no radiological evaluation alone can diagnose rhinosinusitis. Clinical ndings are always more valuable. The diagnosis of uncomplicated rhinosinusitis can be made based on history and clinical ndings. In radiological evaluation, CT and MRI are useful in evaluat­ing cases with chronic or recurrent sinusitis that are clinically considered com­plications [3134].
Rhinosinusitis treatment in children is applied as antimicrobial treatment and supportive treatment for the causative agent. In treating rhinosinusitis, antimicrobial therapy shortens the duration of clinical recovery, especially for the causative agent, and prevents possible complications. In case of antibiotic resistance during treat­ment, it may be necessary to reconsider the following criteria in the history. Suppose the child goes to kindergarten or nursery, has received antibiotic treatment in the last 3months, is less than 2years old, has recently been hospitalized, and has received antibiotic treatment. In that case, there is a high probability of being infected with a Streptococcus pneumoniae strain that has reduced sensitivity to penicillin, espe­cially amoxicillin. If these risks do not exist, amoxicillin is started orally at 45mg/ kg/day. However, if these risks exist, the amoxicillin dose is increased to 80–90mg/ kg/day [35].
As a supportive treatment, the main goal is to reduce edema in the nasal mucosa, open the Ostia, facilitate sinus drainage, and reduce fever. Decongestants, nasal steroids, nasal lavage, and mucolytic drugs are used for these purposes. However, no signicant advantage of these drugs over placebo has been demonstrated. It should not be forgotten that long-term use of decongestant medications can cause rhinitis medicomentosa. The effectiveness of topical steroids in the treatment has been investigated, and it is stated that they may be benecial only for rhinosinusitis caused by allergy. Nasal lavage is helpful in moistening and mechanical cleaning of the mucosa. However, it is challenging to apply to children under two. Pressure nasal lavage should be used cautiously, especially in children under six. Care should be taken in case of acute otitis media because the nasal ora passes to the middle ear via the eustachian tube [3337].

22.6 Adenoid Hypertrophy

Adenoid hypertrophy is essential for nasal congestion and rhinosinusitis in children, especially between the ages of 2 and 6. Adenoid is anatomically located in the pos­terior nasopharynx and is an important member of the Waldeyer Ring. It is essential in developing and maturing non-immune B-lymphocytes, especially in the neonatal period, against environmental antigens during infection processes from the oral cav­ity and pharynx. Adenoid tissue grows in volume until age 6–7 and shrinks and atrophy during early puberty [38].
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The presence of nasal congestion, purulent nasal discharge, postnasal discharge, fever, and cough suggests adenoid hypertrophy and infection. Rhinosinusitis and otitis media may often accompany the condition. Nasal congestion impairs orofacial facial development in the child, causing the typical appearance referred to as an adenoid face. This condition is a result of prolonged nasal congestion. A character­istic adenoid facial appearance with an open mouth appearance, short upper lip, widened nasal dorsum, dome palate, and retrognathic mandible formation can be mentioned in a child who breathes through the mouth instead of the nose [39, 40].
Adenoid hypertrophy in children causes eustachian tubal dysfunction and ear pathologies (serous and recurrent otitis media). In advanced cases, proportional to the degree of nasal obstruction, sleep-disordered breathing and regression in atten­tion and learning skills may be added to the clinical picture [41].
The diagnosis is easily made by history and endoscopic examination (Fig.22.1). Direct radiography has no place in diagnosis; it causes the child to receive unneces­sary radiation. Instead, adenoid hypertrophy can be quickly evaluated with nasal and nasopharyngeal endoscopy. Treatment is surgical removal of adenoid tissue [3941].

22.7 Inflammatory Causes

22.7.1 Allergic Rhinitis
It is one of the most common causes of nasal congestion in children, as a type 1 hypersensitivity reaction mediated by immunoglobulin E due to exposure of the nasal mucosa to the allergen, seen in 6–18% of children [42].
In its physiopathology, it is a picture of inammatory origin, clinically character­ized by watery eyes, itching, nasal discharge (serous), sneezing, and nasal conges­tion, as a result of the nasal mucosa, which has been previously sensitized, that is, encountered with the antigen, facing the same antigen. If the child is not treated early, maxillofacial anomalies may develop due to open-mouth breathing and nasal congestion. While questioning the history, the time when the symptoms appeared, whether they continue seasonally or throughout the year, accompanying cough, sleeping with the mouth open, snoring, sleep quality, growth and development, and nutritional status should be learned. In addition to the ndings, whether there are frequent complaints of acute or serous otitis media or rhinosinusitis should be inves­tigated. Pets and conditions that may cause allergies should be noted [43].
The most common symptom of allergic rhinitis in children is the allergic salute gesture. In this movement, the nose tip is involuntarily pressed upward with the palm to relieve nasal itching and ease nasal breathing. In addition, allergic shiners, which are characterized by the appearance of dark circles on the lower eyelid skin that turn into permanent pigmentation over time, and small half-moon-shaped lines (Dennie-Morgan lines) that appear on the lower eyelid are typical for allergic rhini­tis. Endoscopic nasal examination is critical in the diagnosis of the disease. In endoscopy, mucosa and turbinates are pale, serous discharge is present, and inferior
300
turbinate hypertrophy may also accompany. Additionally, adenoid hypertrophy, antrochoanal polyp, nasal polyp, acute otitis media, serous otitis media, and rhino­sinusitis ndings may also occur [44].
Clinical and anamnesis information is usually sufcient for the diagnosis of allergic rhinitis. Diagnosing and conrming allergy in children, considered in the history and examination, is possible with allergic skin tests. The sensitivity reaction to a specic antigen applied to the skin is measured. In this way, it is determined whether immunotherapy can be used or not [45].
The main goal in treating allergic rhinitis is to protect and stay away from aller­gens. If this is not possible, medical treatment, immunotherapy, and surgical treat­ment can be applied. Surgical treatment aims to include anatomical pathologies such as turbinate hypertrophy, where medical therapy fails, and septum deviation, where it is ineffective [4245].
M. Gümüşsoy and İ. Çukurova
22.7.2 Nonallergic Rhinitis
This group includes all rhinitis in the absence of non-IgE-related immunological mechanisms. It is less common in children and occurs in 70% of adult patients after age twenty [45].
22.7.3 Eosinophilic Nonallergic Rhinitis (NARES)
Nasal congestion and runny nose are the most common symptoms. Although the disease occurs throughout the year, it is more common in autumn and win­ter, when the temperature difference between home and outdoor environments is highest. Sneezing, watery serous runny nose, itching, and symptoms such as nasal congestion are observed. It is a condition in which eosinophils are more than 20% in the smear. Additionally, this disease is characterized by the nega­tivity of the prick skin test and the absence of serum IgE antibodies. It may occur alone or in association with nasal polyps, non-IgE-dependent asthma, or aspirin sensitivity. Corticosteroids are the most critical drug group in treat­ment [46].
22.7.4 Nasal Polyp
It is a chronic inammatory disease whose etiology is not fully explained and is less common in children than antrochoanal polyps. It is often observed on both sides of the nose. Complaints of nasal congestion, runny nose, rhinosinusitis, or allergic rhinitis may accompany patients. Nasal polyps are more common in allergies, asthma, aspirin/nonsteroidal anti-inammatory sensitivity, and cystic brosis (CF) patients. Therefore, nasal polyps in children are a clinical warning sign to investi­gate cystic brosis [47].
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Nasal polyps are seen as pale, transparent, and smooth-surfaced mass lesions during endoscopic nasal examination. Approximately one-third have a unilateral antrochoanal polyp, another third have polyps secondary to the infective process associated with mucus retention that occurs in cystic brosis (CF), and the remain­der are associated with a range of inammatory conditions, although most remain idiopathic. Nasal examination and CT are sufcient for diagnosis and treatment planning. A prick skin test can be performed if there is a history of allergy. Although its treatment is planned medically and surgically, it is sometimes tricky. Corticosteroids are the most critical agents in medical treatment. Endoscopic sinus surgery is preferred in surgical treatment. Management of pediatric polyposis is often disappointing because the recurrence rate is high, except in those with antro­choanal polyps. Therefore, some authors recommend treatment with topical ste­roids as a routine approach in treating nasal polyps and resort to surgery only in case of failure [48, 49] (Fig.22.3).
22.7.5 Antrochoanal Polyp
They are inammatory polyps that originate from the mucosa of the maxillary sinus and extend from the maxillary ostium to the nasal cavity and often to the nasophar­ynx. It has two components: cystic and solid. Antrochoanal polyps are rare in chil­dren but occur at a higher rate than in the adult population. While antrochoanal polyps constitute 4–6% of all nasal polyps, they constitute 33% of the pediatric population. Although it is thought to develop as a complication of chronic inam­matory sinus disease in its physiopathology, studies in the pediatric population have reported that it creates an allergic basis in approximately half of the patients. Unlike adults, allergic polyps are more common than inammatory polyps among children.
Fig. 22.3 Visualization of hypertrophic adenoid tissue from the nasal cavity with exible endoscopy
302
Fig. 22.4 Antrochoanal polyp originating from the left maxillary sinus extends to the middle meatus and then to the nasopharynx on paranasal axial CT
M. Gümüşsoy and İ. Çukurova
Although they often originate from the maxillary sinus, they may also arise from the septum, sphenoid sinus, ethmoid sinus, hard and soft palate, and turbinates. Although they are primarily unilateral, bilateral patients have been reported. They are frequently observed in children and young adults. The main symptoms are uni­lateral nasal congestion, runny nose, and postnasal drip. Computed tomography is the radiological evaluation of choice for evaluating antrochoanal polyps. Classically, they are considered as an opaque hypodense mass originating from the maxillary sinus and extending from the middle meatus to the nasal cavity (Fig.22.4). The treatment is surgery, and endoscopic sinus surgery is preferred. To reduce recur­rence rates, it is necessary to remove altogether the mucosa from which the polyp originates in the maxillary sinus [50, 51] (Fig.22.4).
22.7.6 Inferior Turbinate Hypertrophy
Turbinates are functional anatomical structures important in humidifying and warm­ing the inhaled air. The autonomic nervous system changes the size of the erectile turbinates with sympathetic and parasympathetic stimulation according to physio­logical needs. Inferior turbinate hypertrophy often occurs due to infection or inam­mation caused by allergic rhinitis, vasomotor rhinitis, or infectious rhinitis. In physiopathology, acute or chronic mucosal-submucosal hypertrophy occurs due to congestion. This situation causes nasal congestion and negatively affects the child’s quality of life. Inferior turbinate hypertrophy causes runny nose, nasal congestion, mouth breathing, obstructive sleep apnea, and craniofacial development disorder in children [52, 53].
The endoscopic nasal examination is sufcient to evaluate the hypertrophic infe­rior turbinates and the appearance of the mucosa (pale or hyperemic). As an imag­ing method, paranasal CT is preferred when medical treatment is inadequate, and surgery is considered [54].
22 Nasal Congestion inChildren
In inferior turbinate hypertrophy, nasal steroids, antihistamines, and deconges­tants are used in medical treatment. Long-term drug use in children is challenging and reduces the effectiveness of treatment due to compliance problems. There is no denitive consensus for inferior turbinate surgery in children. Surgery aims to preserve the bone and erectile submucosa of the turbinate while preserving the inferior turbinate mucosa and to maximize nasal airow by reducing nasal tis­sue [55].
Various surgical options have been recently described for treating medically resistant inferior turbinate hypertrophy in children, including laser ablation, submu­cosal microdebrider, and radiofrequency methods. Pediatric otolaryngologists have turned to mucosal protective procedures such as submucosal microdebrider turbi­nectomy and RF instead of turbinectomy, the preferred surgical method [5255].
303

22.8 Neoplasia

22.8.1 Benign Tumors (Juvenile Nasopharyngeal Angiofibroma)
It manifests only in males and typically during adolescence, with recurrent nose­bleeds and unilateral nasal obstruction. Although this is considered a benign tumor, it can be locally invasive. In nasal endoscopy, it is observed as a vascular mass in the posterior lateral part of the middle turbinate at the level of the sphenopalatine fora­men. On endoscopy, it is seen as a light pinkish mass with a supercial vascular structure. Endoscopic nasal examination and radiological evaluation are essential in diagnosis. In cases of clinical suspicion of angiobroma, biopsy is contraindicated due to the risk of bleeding. It is recommended that CT and MRI be evaluated together in imaging. CT is signicant in assessing bone structures. A lobulated, unencapsulated soft tissue mass is typically centered over the sphenopalatine fora­men. The posterior wall of the maxillary sinus may bend anteriorly (Holman-Miller sign). MRI is critical in evaluating the orbital and intracranial spread of the lesion. Treatment consists of primary embolization followed by surgical resection within 48h, usually via an endonasal approach. Recent advances in radiological imaging, embolization, and endonasal surgical techniques and instruments have greatly improved the prognosis [56, 57].
22.8.2 Malignant Tumors
Although malignant nasal masses are rare, they are most commonly seen with nasal congestion and other symptoms such as a change in smell, nosebleeds, nasal/facial pain, nasal asymmetry, swelling, or numbness. Rhabdomyosarcoma, esthesioneuro­blastoma, lymphoma, and squamous cell carcinoma can rarely be seen among other malignant nasal masses with minor salivary glands (adenocarcinoma or adenoid cystic adenomas), which can lead to the development of salivary gland tumors in the nasal cavity mucosa [58].