The diagnosis of pediatric rhinosinusitis often proves challenging due to the overlap of the symptoms of this disease with various other nasoadenoidal problems, including the common cold. The confusion exists because rhinosinusitis is part of a continuum of disease. Most cases of rhinosinusitis in children actually begin as a viral upper respiratory infection (URI) in the nasal mucosa, eventually progressing to a secondary bacterial infection involving the paranasal sinuses.^{1, 2}

The continuum of disease theory explains why rhinosinusitis cannot be differentiated from viral rhinitis on clinical grounds alone, and why isolated rhinitis probably exists, yet isolated sinusitis is rare.³ Because of the resulting inconsistencies in the interpretation of a child’s symptoms, the management of pediatric rhinosinusitis itself is often inconsistent.

Further confounding the assessment and management of this disease is the fact that the natural history of chronic pediatric rhinosinusitis is not well understood. Thus, as opinions regarding etiology vary, so do opinions regarding appropriate treatments. The therapeutic spectrum ranges from no intervention, to maximal medical management, to aggressive surgical intervention. At the conservative end are those who support minimal to no intervention. This is based on evidence that argues that spontaneous resolution of chronic pediatric rhinosinusitis is the norm.^{4, 5} At the other end of the spectrum are those favoring earlier surgical intervention. Controversies, however, still revolve around the definition of maximal medical management, clear indications for surgery, the extent and timing of surgery, postoperative care, and potential surgical risks. Although advances are being made in understanding this disease process, data directing management is still limited. There are no prospective studies to date comparing medical with surgical therapy in this population to serve as a decision-making guide.

Embryology and Anatomy

In children, the precise anatomy of the paranasal sinuses is complex and quite variable, however, some consistencies do exist. There are four groups of paranasal sinuses: maxillary, ethmoid, frontal, and sphenoid. All the paranasal sinuses develop as nasal chamber outpouchings, eventually extending into their respective bony vaults to varying degrees. The paired maxillary sinus develops early during the second trimester of fetal life and is fully developed by 3 years of age, up to which time the respective cavities are growing in width and height.^{3, 6} Ultimately, the floor of the maxillary sinus is determined by the eruption of teeth.

The ethmoid sinus develops during the fourth gestational month, although matures at a slower pace than the maxillary sinus. The ethmoid sinus exists as paired groupings of individual cells or compartments subdivided anatomically on the basis of their locations, usually with 5 to 15 cells per side.³ Aeration of ethmoid cells is variable, producing a honeycombed radiographic appearance. The thin lateral walls of the ethmoid labyrinth are intimately related to the medial orbit.

Development of the typically paired frontal sinus is quite variable. After 4 years of age, the frontal sinus is in a supraorbital position; however, it is radiologically indistinguishable from the ethmoid sinus until 6 to 8 years of age. Growth then continues for another 8 to 10 years before reaching full adult development.³ The sphenoid sinus is present at 3 years of age and is generally fully developed by 12 years of age. Its slow growth and relative isolation in the skull base may preserve it from frequent infection, as isolated sphenoid sinusitis is uncommon in children.³

Physiology and Pathophysiology

The paranasal sinuses and their pathways are lined by mucosa composed of ciliated pseudostratified columnar epithelium. The cilia beat consistently in a fluid medium, moving sinus secretions out toward the natural ostia, along the drainage pathways, and eventually into the nasopharynx. It is this interplay of ostial patency, mucociliary functioning, and fluid secretions that allows for normal paranasal sinus physiology. When one or more of these elements is impaired, the potential for sinus dys-function exists.

Patency of the paranasal sinus ostia with maintenance of drainage pathways is a key element in normal sinus physiology. The posterior ethmoid cells drain secretions through the superior meatus, and the sphenoid sinus drains into the sphenoethmoidal recess. The frontal sinuses, anterior ethmoid sinuses (agger nasi cells and both supra- and infraorbital ethmoids), and maxillary sinuses drain into the osteomeatal complex (OMC). This area consists of the hiatus semilunaris, frontal recess, anterior ethmoid cells, ethmoid bulla, anterior wall of the middle turbinate, and the infundibulum. The infundibulum is a troughlike space just anterior to the anterior ethmoid cells, which acts as a common drainage pathway. Because of these anatomic and physiologic relationships, OMC or anterior ethmoid disease can induce mucosal edema and functional obstruction of the infundibulum and drainage of its related sinuses.⁷ Mechanical factors, as well as functional factors, may also precipitate obstruction, although viral URI with secondary mucosal swelling is by far the most frequent cause of ostial obstruction.³

Once the sinus ostia become obstructed, ventilation is impaired and there is a transient increase in intrasinal pressure, followed by a negative intrasinal pressure.8 The negative pressure within the sinus relative to the atmospheric pressure may allow nasal flora to flow against the mucosal ciliary beat patterns and enter the typically sterile sinus cavity. Sniffing, sneezing, and nose-blowing, associated with altered intranasal pressure, may also facilitate entry of bacteria into the sinus from a colonized nasal chamber.³ As nasal congestion increases, nasal breathing decreases; decreased gas exchange produces a decreased partial pressure of oxygen intrasinally, which favors multiplication of certain bacterial species. An acidic pH may also develop, promoting anaerobic conditions. As the immune system responds to the bacterial invasion, tissue congestion worsens secondary to the inflammatory response, further perpetuating the cycle of obstruction.

Normal mucociliary functioning usually protects respiratory epithelium from bacterial invasion, however, certain respiratory viruses appear to exert a direct cytotoxic effect on the cilia.³ Alteration of the number, morphology, and function of cilia in the respiratory epithelium may facilitate secondary bacterial infection of the paranasal sinuses. Ciliary activity may also be impaired with alterations in mucosal secretions, as cilia can only beat in a fluid medium. Thickened secretions typically seen in systemic disorders such as cystic fibrosis or asthma have the potential to impair ciliary movement. Purulent secretions from an infected sinus may also affect ciliary movement, however, reports on this are conflicting.^{9, 10}

Ostial obstruction thus initiates a vicious circle, with self-mediated mucosal edema and hyperplasia, obstruction of sinus drainage, retention of secretions, and ciliary dysfunction, cumulatively creating an environment ideal for long-standing infection. In children, OMC obstruction is recognized as a critical factor in chronic rhinosinusitis, however, it is unclear whether this is the primary cause of the disease.

Perhaps critical to our further understanding of this unique pathophysiologic model is the concept that there is rarely a single isolated cause. A number of conditions have been identified as predisposing to chronic rhinosinusitis in children, although an acute viral illness—the common cold—appears to be the most frequently recognized association.^{11, 12} Data suggest children average 6 to 8 upper respiratory infections (URIs) per year, and acute sinusitis complicates 5 to 10% of cases.^{13, 14} The precise mechanism whereby viruses predispose to rhinosinusitis is unknown, but it may involve local immune defense destruction and a subsequent increase in bacterial attachment to epithelial cells.¹⁵ An immature immune system and lack of previous exposures presumably make children more susceptible to common viral URIs, especially in settings where close contact with other children facilitates infectious transfers.¹⁶ Also, the smaller size of developing sinuses and a shorter distance between ostial mucosal surfaces may further facilitate OMC obstruction, and encourage the development of rhinosinusitis after a viral URI in children.¹⁶ Potentially modifiable predis-posing factors involved in the pathogenesis of this disease have also been identified, and are addressed later in the chapter.

Definitions

According to the most recent consensus meeting in Brussels,¹⁷ chronic rhinosinusitis in children is defined as a sinus infection with low-grade symptoms and signs that persists for longer than 12 weeks. This definition allows for a diagnosis without the previously mandatory computed tomography (CT) scan, based on the consensus panel’s belief that imaging all children with suspected chronic rhinosinusitis is not feasible.¹⁷ Patients with acute exacerbations of chronic rhinosinusitis may have multiple acute episodes in addition to persistent low-grade symptoms and signs that do not resolve completely between acute episodes.

Symptoms and Signs

A thorough history is the most critical component in the evaluation of rhinosinusitis. Symptoms most commonly associated with chronic rhinosinusitis in children have been described by Parsons and Phillips as “the seven cardinal symptoms.”¹⁸ These include chronic nasal congestion (100% occurrence), purulent nasal discharge (90%), head pain/discomfort (90%), cough (71%), fetid breath (67%), postnasal drainage (63%), and behavioral changes (63%).¹⁸ The cough, most often secondary to postnasal drainage, is typically worse in the evening for younger children, and in the early morning for adolescents. Infrequent symptoms reported in less than 20% of the study population include recurrent odynophagia, intermittent fever, nausea, hoarseness, facial puffiness, epistaxis, dizziness, impaired smell, epiphora, and localized pain in the ear, eye, or maxillary teeth.^{18, 19}

A complete head and neck examination should be performed in all children with suspected rhinosinusitis. It is especially important to rule out other possible etiologies of a child’s symptoms, such as adenoid hypertrophy and obstruction, foreign body, tumor, choanal stenosis or atresia, and deviated nasal septum.⁷ On physical examination, the signs of chronic rhinosinusitis are not specific, and there are no direct means of examining the paranasal sinuses. The examination itself is challenging in the pediatric patient, but it may be accomplished in a simple way by tilting the tip of the nose upward. Anterior rhinoscopy with the use of an otoscope provides even better visualization. These methods permit assessment of the inferior (and possibly middle) turbinate and mucosa; the nasal septum; the presence or absence of crusts, secretions, and lesions; and the overall patency of the nasal airway.²⁰ Findings suggestive of rhinosinusitis include boggy edematous mucosa with significant obstruction, along with various amounts and types of nasal discharge. Other physical findings may include cobbling of the posterior pharyngeal lymphoid follicles, posterior nasal discharge, and slightly tender enlarged cervical lymph nodes.^{7, 21} Intranasal polyps are principally seen in association with cystic fibrosis or allergy.³ Investigators also report widening of the nasal bridge in some children with chronic rhinosinusitis, producing a pseudohypertelorism.3

Although virtually impossible in the very young child, nasal endoscopy can sometimes be performed in patients 6 years of age or older. It is helpful to prepare the nose first with a topical decongestant (0.25% phenylephrine) and topical anesthetic (3% lidocaine) administered via an atomizer. The 0- and 30-degree rigid pediatric endoscopes provide the most complete view of the nasal mucosa, nasopharynx, and middle meatus and enable the clinician to obtain cultures and tissue samples in select cases.

Flexible nasopharyngoscopy is better tolerated and allows good visualization of the nasal cavity and nasopharynx; this method, however, does not yield sufficient information about the middle meatus, which is the site of the osteomeatal complex, a key concept in the pathophysiology of rhinosinusitis.²²

Diagnosis

The most commonly used basis of diagnosing chronic pediatric rhinosinusitis is clinical judgment. Transillumination of the sinuses in children is difficult to perform and unreliable, especially in patients younger than 10 years of age because of increased thickness of both the soft tissue and the bony vault.^{3, 23} The value of ultrasonography is controversial, and has a very limited or no role in evaluating rhinosinusitis in children^{20, 24–26} Similarly, plain radiographs have limited value in this setting;²⁷ interpretation in infants and young children is often difficult, there is poor correlation with ethmoid disease, and the significance of sinus clouding is uncertain.²⁸ Furthermore, plain sinus films do not provide visualization of the osteomeatal complex, a cornerstone in the diagnosis of rhinosinusitis.¹² In a study comparing plain sinus films with coronal CT scans taken within hours of each other in children displaying symptoms compatible with chronic rhinosinusitis, there was a lack of correlation between the two methods in 74% of the patients.²² The investigators concluded that plain films both over- and underestimate sinus findings.²² Radiographic examination of the nasopharynx, however, may be adjunctively helpful in determining the size of the adenoids, yet this does not replace nasopharyngoscopy; adenoidal tissue size alone does not necessarily correlate with chronic inflammation.¹⁵

Imaging is not necessary to diagnose uncomplicated pediatric chronic rhinosinusitis. When indicated, however, fine-cut coronal CT is the imaging modality of choice because of its ability to resolve both bone and soft tissue.²⁹ The need for caution when considering CT evaluation must be emphasized, as the incidence of bony or mucosal disease of the paranasal sinuses in asymptomatic children may be as high as 50% on imaging.³⁰,³¹ In children with symptoms and signs compatible with chronic rhinosinusitis, CT scanning is most frequently performed if surgery is being considered, or if the patient has a complicated course or a systemic disorder. According to the Brussels consensus meeting, the complete list of indications for CT scanning in the assessment of pediatric rhinosinusitis includes:¹⁷

1. 
   

   Evaluation of the surgical candidate

   
   
2. 
   

   Presence of suppurative intraorbital or intracranial complications (excluding orbital cellulitis)

   
   
3. 
   

   Symptomatic immunocompromised host

   
   
4. 
   

   Severe illness or toxic condition

   
   
5. 
   

   Acute illness that does not improve with medical therapy in 48 to 72 h

In comparison to CT, magnetic resonance imaging (MRI) provides optimal visualization of soft tissues but has no bone resolution. This imaging modality thus has no use in routine evaluation of the paranasal sinuses, and cannot be used reliably as a preoperative guide. MRI is most often reserved for children with suspected neoplasm, congenital mass, intraorbital/intracranial complications, or intravenous contrast allergy.^{32, 33}

Microbiologic assessment is not necessary in cases of routine evaluation of uncomplicated chronic rhinosinusitis in children, although it does have a role in recalcitrant and complicated disease. Results of most surface cultures have no predictive value, and thus nose, throat, and nasopharyngeal cultures cannot be recommended as guides to the bacteriology on therapy for chronic rhinosinusitis.²⁵ Cultures of pus taken directly from the middle meatus do, however, correlate well with maxillary antral and ethmoid cultures,^{34, 35} although there is no consensus regarding whether middle meatal cultures can substitute for sinus aspirations.¹⁷ Indications for maxillary sinus aspiration or puncture in children parallel indications for CT scanning and include symptomatic sinus disease in an immuno-compromised host, suppurative complications, severe illness or a toxic condition, and acute illness unresponsive to therapy within 48 to 72 h.¹⁷ This technique is best performed transnasally to avoid injury to dentition and the natural ostium. After sterilization of the puncture site, a needle on a syringe is directed beneath the inferior turbinate and advanced through the lateral nasal wall.² Aspirated secretions are submitted for gram stain and aerobic and anaerobic cultures. Bacterial counts of greater than 10⁴ colony-forming units (CFU) ml reflect a high degree of confirmation of infection, rather than contamination.³

Predisposing Factors

Chronic pediatric rhinosinusitis is recognized as a multifactorial disease with various predisposing factors that change over time. Once the diagnosis of rhinosinusitis is suspected in a child, underlying modifiable contributors to sinonasal inflammation must be identified and managed appropriately. Once this is accomplished, the infectious disease aspect which actually may be secondary, can then be more effectively treated.⁷ Although their roles are still being defined, conditions that are currently recognized as potential predisposing factors for rhinosinusitis include allergy,²⁷ immunodeficiency,^35–38 cystic fibrosis,^{39, 40} primary ciliary dyskinesia,^{41, 42} environment,^{43, 44} and gastroesophageal reflux.^45–47

Allergy is one of the most common causes of problematic nasal mucosa edema48 and is implicated as a contributing factor in rhinosinusitis.⁴⁹ Some investigators consider allergy in children the most important predisposing element in pediatric chronic rhinosinusitis,^{50, 51} although its true role in this disease process is still under debate. Controlled studies comparing the incidence of sinusitis in allergic groups with nonallergic groups are very scarce, especially in pediatric populations. One study found no difference in the involvement of the sinuses of atopic children in comparison to nonallergic children with chronic nasal complaints.⁵² The same investigators showed the prevalence of rhinosinusitis to decrease after 8 years of age, and the prevalence of atopy to increase with age.⁵² Together, these findings suggest that allergy may not be a primary cause of chronic pediatric rhinosinusitis.⁴⁴ Interestingly, however, the prevalence of rhinosinusitis in allergic children is higher than in nonallergic patients.^{44, 53}

Identification of the allergic child is important in patient evaluation, and a complete medical and family history is the most critical aspect of this process. Symptoms suggestive of allergy include nasal congestion, pruritic nasal and ocular mucous membranes, clear rhinorrhea, paroxysmal sneezing (often exacerbated by inhaled dust or animal exposure), and rhinosinusitis during allergy season.^{17, 27} The history may also include infantile eczema, asthma, food allergy, or a previous good response to antihista-mines or intranasal anti-inflammatory agents.¹⁷ Family history is important because children of two allergic parents have a 65 to 75% incidence of significant atopy, and children with one atopic parent have a 35% incidence of allergy.⁵⁴ The likelihood of allergies is also increased in children with an atopic sibling.⁵⁴

If any elements of the history or physical examination suggest atopy, allergic assessment should be performed.¹⁷ Some investigators assert that allergy testing should be obtained in every child with chronic rhinosinusitis who responds poorly to initial management, regardless of whether the history is positive for atopy.⁴⁸ This is based on the high occurrence rate of allergic disease in rhinosinusitis patients.⁴⁸ Acceptable methods of assessment include skin-prick testing, nasal smear, radioallergosorbent testing, or treatment trials.¹⁷ Intradermal skin testing is reported to be the most sensitive study, but some in vitro blood tests have been found to be accurate within 5 to 8% of the intradermal results.^{48, 55}

IMMUNODEFICIENCY

Young children all have a relative physiologic immunodeficiency because of a slow continual rise in plasma immunoglobulins (IgG, IgM, IgA) until 6 to 10 years of age, when adult levels are finally reached.²⁹

Stay updated, free articles. Join our Telegram channel

Join