A globally prevalent disease, chronic rhinosinusitis (CRS) may be defined as a multifactorial inflammatory and infectious disorder involving the nasal mucosa and paranasal sinuses, with symptoms persisting for longer than 12 weeks. An expensive, long-term process with a high risk of complications, CRS is often refractory to treatment. As one of the most common diseases of childhood, CRS has a significant effect on a child’s quality of life, mostly through bodily pain and limitation in physical activity.1,2 Pediatric CRS appears distinct from the adult form of the disease, based on anatomic, histologic, and immune particularities and the effect of certain predisposing factors/comorbidities on this condition in childhood.2
Pediatric CRS is more frequently diagnosed between the ages of 4 and 7 years, whereas acute rhinosinusitis usually affects 1- to 5-year-old children. The exact incidence of pediatric bacterial sinusitis is unknown. However, it may be inferred indirectly from the frequency of six to eight upper respiratory infections (URIs) children have every year, with 5% to 13% of these infections becoming acute bacterial rhinosinusitis.3 In adults, only 2.4% to 7.5% of acute rhinosinusitis become CRS.4,5 Similar information specifically for the pediatric group is not available.
A recently published cross-sectional study of 42.1 million school-aged pediatric patients found a 4% annual incidence of CRS, corresponding to an affected 1.7 million school-aged children.6 A survey estimates the prevalence of CRS in the general population to be 2.7% to 6.6%, with an increase with age.7 The exact prevalence of CRS in children is difficult to determine because only a small percentage of cases present to the physician’s office.1 Moreover, this condition is often overlooked in pediatric practice, which may lead to lack of adequate management.
Difficulties of Diagnosis
Multiple challenges face the physician in the quest to diagnose CRS. Variations in the definition of CRS reflect our incomplete understanding of the exact nature of this condition. Although its inflammatory nature is increasingly recognized as the main characteristic, the role of bacterial involvement, as well as that of the initiating events of the host susceptibility and environmental factors in the pathogenesis of the condition, remain largely unknown.
Similar to the adult form, diagnosis requires identification of two or more symptoms, one of which should be either nasal blockage/obstruction/congestion or nasal discharge; cough and facial pain/pressure may be present. Either objective signs of the disease on the physical examination (including an anterior endoscopy) and/or relevant changes on computed tomography (CT) scan of the sinus need to be added (Table 1).
Diagnosis of Pediatric CRS
However, accurate diagnosis of pediatric CRS is difficult because children present with more nonspecific, subtle symptoms than adults. Physical examination may be unremarkable or difficult to perform optimally if the patient will not tolerate nasal endoscopy and because imaging procedures in this age group are generally discouraged.3
Meanwhile, children have frequent URIs, may get adenoid hypertrophy, and are prone to allergic rhinitis, all diseases with similar symptoms to CRS. Hence, it is hard to tell where one pathology ends and where another begins.1 A common scenario is children presenting as acute recurrent sinusitis such that the chronic nature of the disease may be missed. A form of CRS may present as acute recurrent acute sinusitis or repeat otitis media with effusion, which may deter from the correct diagnosis.8 Suspicion of CRS in pediatric patients may be decreased by the occasional belief that paranasal sinuses are not yet developed in the small child.9
Anatomy and Pathophysiology
The paranasal sinuses are air-filled cavities in the bones of the head that communicate with the nasal passage through tubular openings (ostia). They are lined with a ciliated epithelium that sweeps mucus toward the ostia. The maxillary and ethmoid sinuses are the most commonly involved in young children’s sinusitis and are present at birth. Their complete pneumatization is reached at approximately 12 years. Sphenoid sinuses develop at 3 years, and frontal sinuses appear at 7 years.
Pneumatization of these sinuses is completed in mid to late adolescence. The frontal sinuses may be underdeveloped in 15% of the population, and the sphenoid sinus is hypoplastic in 26% of the population.3 The prevalence of sinusitis increases after 6 to 8 years, marking the addition of the frontal sinuses as yet another site that can be affected by rhinosinusitis.3,7 A decrease in the prevalence of CRS after ages 6 to 8 was reported by researchers and is an additional area of controversy.1
Keeping Sinuses Healthy
Normal function of the sinuses requires that the ostia remain patent, the mucociliary function is normal, and the systemic and local immunity responses are appropriate. When all of these work well, sinuses remain sterile, and transient, low-density bacterial contamination is dealt with effectively.
Origins of Disease
A defective mucociliary clearance, blocked-off sinus drainage, or large microbial threat close to the sinuses may act individually or in combination to lead to the development of CRS.
Ostium patency is affected by mucosal inflammation of any type or by mechanical obstruction. The mucosa in the nasopharynx and overlying adenoids and tonsils may harbor bacterial aggregates of more than 104 CFU/mL,9 constituting the source of infection for nearby sinuses.
Blocked mucus drainage through the sinus ostia decreases oxygenation and increases the acidity inside the sinuses. These local conditions facilitate bacterial growth. Once purulent secretions form, they further contribute to the decrease of oxygenation in the sinuses.3
However, CRS does not result simply from obstruction to sinus drainage and exposure to microorganisms. The nasal epithelium reacts inappropriately to pathogens, both with regard to the local immunity and the recruitment of adaptive immune responses, which become persistent and produce the clinical symptoms of CRS.10,11
Role of Inflammation
Biopsy samples of CRS show intense inflammation with eosinophils, neutrophils, and lymphocytes, as well as T-cell–produced cytokines and chemokines, in response to allergens, irritants such as ozone or cigarette smoke, or exposure to bacterial superantigens. Regardless of the inciting factor, the elevation in cellular constituents in CRS points to a vigorous immune response.10
The effects of the released mediators are vasodilatation, increased mucus secretion, neurogenic inflammation, and mast cell–nerve interactions. The resulting inflammation leads to local changes that favor the development of infection, as previously described. Inflammation and infection engage in a cycle that may explain, in part, the protracted nature of CRS.2
Samples of sinus mucosa in young children (1 to 8 years) with CRS show a lymphocytic infiltrate unlike in the adult, where eosinophils and neutrophils prevail.12
The eosinophilic remodeling with thickened basement membrane and submucosal gland hyperplasia seen in the adult is not yet present in the young child with CRS. These morphologic changes become apparent only in the older child, suggesting that there may be a progression of sinus tissue damage from the very young to the adult type of CRS. Early diagnosis and treatment may prevent the long-lasting changes typical for CRS.12 Extensive fibrosis was found in samples from children with higher cellularity, in the absence of eosinophils, raising yet another question about the particular nature of pediatric CRS.13
Elements of Infection
CRS used to be thought of essentially as an infection of the sinuses. Paralleling the recognition of its inflammatory nature, there was increasing doubt about the role of infection in CRS. This may be partly caused by difficulty identifying any pathogens on nasopharyngeal cultures and the less-than-optimal effect of antibiotics that, in the absence of culture and sensitivity guidance, are being used empirically.14 Even when positive cultures are obtained, contamination with colonizing bacteria is suspected.
In a more integrated perspective, numerous factors contribute to CRS, including infection because it causes inflammation. The lack of success in treating CRS with antimicrobials is explained by the fact that CRS is managed as a planktonic (free-floating) bacterial infection. However, ample evidence shows biofilm to be present in surgically removed sinus mucosa from patients with CRS.15
Biofilm in Infection
A bacterial biofilm consists of a complex colony of microbial cells that live within a self-produced polysaccharide matrix and are strongly adherent to surfaces, such as respiratory mucosa. Microorganisms cross-talk, a process called “quorum sensing.” The gene expression is different from the planktonic state of the same bacteria, and metabolic requirements are reduced.16 These adaptations render the biofilm bacteria more resistant to antibiotics and to killing by immune factors. The reservoirs of biofilm for sinuses are the adenoids, tonsils, and nasopharyngeal mucosa.
Biofilm pathogen identification requires special tests, usually done in research. Antibiotics best suited for biofilm may need different characteristics than those effective on free-floating bacteria. Biofilms associated with CRS are typically polymicrobial, commonly including Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus pneumoniae, coagulase-negative staphylococci, Moraxella catarrhalis, Haemophilus influenzae, anaerobes, and even fungi.1,17
A review of the presenting symptoms of CRS (Table 1) underscores the often nonspecific symptomatology in children. Pediatric CRS may disguise as URIs, otitis media, and slow growth. The symptoms are relatively age dependent. Very young children show irritability, easy fatigability, and poor eating. Young children may vomit from gagging on mucus or from coughing; they may snore, have a restless sleep, sleep in abnormal positions, or have apnea. They get sore throats on awakening and epistaxis.
The main complaints in older children may be general malaise, poor school performance, and decreased attention span, which turn out to be caused by sleep deprivation. Fever and headaches are less common in pediatric CRS.
Findings on physical examination may be subtle and nonspecific, creating a challenge in diagnosis. On inspection, mouth breathing, coughing, abnormal voice, and halitosis may be noted. Percussion of the sinuses is rarely useful in children.
Examination with the otoscope is difficult in young children, but when it can be done, it may reveal anatomical obstructions and masses, such as polyps and foreign bodies. The turbinates may be swollen and red. Nasal mucosa does not have the normal pink-orange color with slight sheen that indicates good hydration. Mucopurulent to colorless secretions may be present in various amounts or may be absent.
Foul-smelling mucus is often associated with a foreign body that has been placed into the nose. Concomitant erythema of the oral pharynx and signs of otitis media are common in CRS. Periorbital edema is more typically associated with ethmoid sinusitis.3,7,9,18
Complications occur rarely in CRS but include orbital infections or intracranial spread of the infection. Patients with these complications may experience severe consequences, including visual impairment, neurological deficit, or death. The diagnosis of these complications may be delayed because symptoms continue to resemble those of sinusitis.1,18,19
CRS may be described as a dysfunction of host environment at the site of interaction in the nose and sinuses. It is unclear whether host factors (systemic and local) and environmental conditions that affect CRS induce the disease or if they share a common pathway of pathogenesis with it. Following is a listing of these factors.
Viral URI is the most common predisposing factor for bacterial sinusitis. Attendance in day care facilities triples the incidence of URI.3,20 Viral rhinosinusitis causes nasal obstruction and abnormal mucociliary activity.6 Symptoms that persist for weeks and months after a viral URI should raise the consideration for an ongoing CRS. Increased exposure to infectious microorganism (bacteria, fungi) heightens the risk of superimposed secondary infections.
Unopposed growth of pathogens during respiratory illnesses may be due to the absence of nonpathogenic organisms that colonize the nasopharynx in healthy individuals. These organisms play a role of bacterial interference, thus potentially preventing the development of sinusitis.21
Environmental exposure to tobacco smoke inhibits mucociliary clearance and epithelial regeneration. Smoking parents harbor fewer favorable interfering bacteria and are a source of pathogens that may colonize and infect their children’s respiratory tract.20 Noxious inhalants, such as ozone, chlorine, and other pollutants, present as small particulate matter may irritate the nose and sinuses.22
Allergic inflammation alters the sinonasal physiology with regard to mucociliary clearance and ostiopatency. A late-phase allergic inflammation may contribute to CRS development.
Immunotherapy for allergic rhinitis has been shown to help in CRS.9 However, some data support and some deny an important role of allergy in CRS development.23 Overlapping symptoms make it difficult to differentiate between the two conditions.
According to some studies, the prevalence of sensitization to aeroallergens in CRS patients is approximately the same as in the general pediatric population, whereas other studies show a higher percentage of atopy in patients with CRS compared with the general population.23 Allergic-type inflammation (elevated immunoglobulin E [IgE]; presence of interleukin-4, -5, and -13) was found even in the non-allergic CRS patients.1,24 The lack of positive association between atopic conditions and the presence of CRS in children may suggest that infectious etiologies play a more significant role rather than inflammation alone in the pathogenesis of this disease in pediatric patients.24
Local Allergic Rhinitis
Studies may have failed to show a significant association with local allergic rhinitis because some patients have local nasal allergy without positive skin tests or serum IgE elevation. These patients have clinical criteria of perennial or seasonal allergic rhinitis. Positive nasal allergen provocation tests may prove the correlation.
In some studies, nasal provocation tests were positive to dust mite allergen in 54% of patients thought to have idiopathic rhinitis. Nasal provocation tests were positive to seasonal allergens in 62.5% of patients with rhinitis and negative skin tests.23 It appears that local B cells in the nasal mucosa become sensitized and produce specific IgE that binds to local mast cells.25
Approximately 17% to 52% of CRS is associated with nonallergic rhinitis. This has a 5% to 10% prevalence in the general population.6 Rhinitis triggered by allergic and nonallergic factors is considered mixed rhinitis.3
Allergic Fungal Rhinitis
The role of fungi in the pathogenesis of CRS is unclear. Fungi are present in the air at all times and are found in the normal nose. Allergic fungal rhinosinusitis (AFRS) is a noninvasive form of CRS caused by a hypersensitive reaction to the inhaled fungi. It is the most common form of fungal CRS in children.26
All children with AFRS are atopic, and almost all have nasal polyps. In children with unilateral asymmetrical nasal polyps, facial abnormalities, or proptosis, AFRS should be considered.27
Asthma is noted in frequent association with rhinitis; 80% of children and adolescents with asthma have rhinosinusitis, and 40% of children with CRS have asthma. Asthma and CRS can amplify each other, and they show correlating severity. Treatment of CRS was shown to improve bronchial hyperreactivity.28 It is unclear how exactly the two conditions interact.
Cough is often thought to be a symptom of asthma. However, in one-third of patients with a nocturnal cough, it is not asthma but CRS that causes the symptom. Chronic cough is a main symptom of CRS in children. The widely embraced concept of cough-variant asthma may decrease the likelihood of pediatricians making the diagnosis of CRS.9,27,29
Immunologic incompetence or immaturity may contribute to the pathophysiology of CRS in children. CRS, usually without polyps, is the most common complication of common variable immunodeficiency (75%).23,30 Immune compromise secondary to chemotherapy in children is associated with an increased incidence of CRS and invasive fungal sinusitis in these patients.
Immunodeficiency is usually suspected when a patient has recurrent pulmonary infections and otitis media in addition to CRS, or when their CRS is poorly responsive to usual therapy.26
Otitis Media With Effusion
Otitis media is often a presenting symptom of CRS. Radiologic abnormalities in keeping with CRS were found in patients with otitis media refractory to treatment in half of patients aged 10 to 20 years and in almost 80% of 4- to 9-year-old children.31
Because the middle ear has an anatomic and functional connection with the nasopharynx through the eustachian tube, the middle ear cavity is also a paranasal sinus. The nasal mucosa inflammation may cause obstruction of this sinus ostia (ie, the eustachian tube opening), leading to its dysfunction. Consequently, the middle ear pressure is impaired, and fluid exudates.19
Gastroesophageal reflux disease (GERD) is related to CRS in some pediatric patients, but its association with respiratory disease and its incidence remain in doubt. Data are conflicting. Gastroesophageal reflux is a physiological phenomenon at age 3 to 4 months. It is naturally decreasing thereafter, but it is still present in 20% of infants. Pharyngeal reflux is documented in half of these children.32 Fifty percent of normal children regurgitate until age 2 years; meanwhile, CRS is seen mostly in those older than 2 years.18
On the other hand, studies have shown that esophageal reflux occurs in 63% of CRS sufferers and in only 5% of the general population.33 Nasopharyngeal reflux was demonstrable in one-third of children in the CRS group. Treatment of GERD resulted in significantly improved sinus symptomatology for most patients, even when nasopharyngeal reflux was not demonstrated. In another study, therapy of coexisting gastroesophageal reflux in children with refractory CRS obviated the need for sinus surgery.34
The clinical diagnosis of GERD is difficult because children rarely complain of typical symptoms of heartburn, sour eructations, or regurgitations. They have less specific manifestations, such as nausea and decreased appetite.33
Reflux of gastric acid into the pharynx and nasopharyx is thought to cause sinus ostium inflammation, impaired mucociliary clearance, and, consequently, sinusitis. Until the strength of the association between CRS and GERD is validated, routine anti-reflux therapy of children is not warranted.1
Cystic fybrosis (CF) is an autosomal-recessive disease caused by a gene mutation that leads to formation of thick viscous secretions favoring infections in the respiratory tract. P aeruginosa and S aureus are the microorganisms most frequently cultured when the biofilm infection sets in the sinuses.23
Nasal polyps are rare in children, but 5% to 86% of children with CF have nasal polyps.23 Even in the absence of symptoms, most patients with CF have chronic sinus inflammation. The prevalence of CRS is increased even in heterozygotes when compared with nonmutated subjects.23 CRS is usually severe. CF should be considered in children with nasal polyps or with CRS appearing at an early age.3,23
Local Host-Related Factors
The prevalence of CRS in the absence of systemic immune defects may be explained by subtle abnormalities in the innate defense at the level of the sinonasal epithelial cells. Mucociliary clearance is the primary mechanism of defense at the site. Primary ciliary diskinesia is a rare genetic disease in which the sinonasal cilia are reduced in number and have abnormal morphology and function.15,18
Mucociliary dysfunction may otherwise occur secondarily to infection. The morphology of cilia may become abnormal in the context of CRS itself, contributing to the self-perpetuating nature of the disease. Loss of ciliated epithelial cells occurs in rhinitis medicamentosa induced by topical decongestants, explaining the delay in a return to normalcy of the sinonasal mucosa even after discontinuation of the vasoconstrictor drugs.
Epithelial cells express toll-like receptors and produce antimicrobial peptides. Hence, they can detect bacterial presence and kill pathogens directly, a further contribution to the local innate immunity.1 Any defects of the ciliated epithelial cell may predispose to infection.
Anatomic abnormalities that cause nasal obstruction may be conducive to unilateral or bilateral sinusitis. Septal dislocation caused by birth trauma, unilateral choanal atresia, nose fractures, foreign body in the nose, septal deviation, infraorbital Haller cells, or concha bullosae (middle turbinates aerated from the ethmoids) can cause blockage. Recently, the cause-effect correlation of these anatomic abnormalities and CRS has been called into question.1 Hypertrophic adenoids, enlarged tonsils, and polyps may be obstructive. Polyps are infrequent in children, except those with CF.3,14,26 Dental infections may spread into the sinuses, causing odontogenic sinusitis.14
A family history of asthma or inhalant allergies appears to be a risk factor for the development of pediatric CRS.18,30,32
Challenges in Diagnosis
The diagnosis of CRS is primarily a clinical one, based on history and physical examination. The diagnostic criteria for pediatric CRS follow guidelines defining adult CRS. These recommended the diagnosis of CRS be made in those patients exhibiting the most common rhinosinusitis symptoms lasting longer than 12 weeks in association with other endoscopic or imaging evidence.1
In children, symptoms are different than in adults, with cough as the most common presentation. Physical examination may be suboptimal, and imaging criteria is useful but not an absolute necessity and not usually obtained.
The history should elicit information on specific symptoms and patterns of symptoms to assess exacerbations and complications, precipitating factors, existing comorbid conditions, environmental exposure, personal and family medical history of atopy, and response to therapy. A particular challenge for the pediatrician is to differentiate true CRS from frequent URI, adenoiditis, or perennial allergic rhinitis with overlapping manifestations.
A handheld otoscope or a head lamp with nasal speculum is usually appropriate for a nasal examination to look for purulent discharge, swelling, and other mucosal changes. Nasal endoscopy may be difficult in young children because it requires cooperation. In older children, it may be satisfactorily performed after a topical decongestant and local anesthetic spray.3
Transillumination of sinuses is not reliable. It may be useful only if complete opacification is present.
Sinus radiographs are discouraged, except for exceptional circumstances. Sinus radiographs are insensitive, with many false positive and false negative results. Only the Caldwell and Waters views are helpful in children younger than 4 years; lateral views may be added for children older than 4 years. Sinus radiographs are technically difficult if the child is uncooperative or if positioning is incorrect.3,18,19
A CT scan is not necessary for diagnosis. It is the imaging modality of choice only in presurgical cases. The radiation doses delivered are higher than plain radiographs—hence a concern for children.3,19 The American Academy of Pediatric Section on Radiology states that “pediatric health care professionals’ role is to decide when CT is necessary and to discuss the risk with the patient and family.”8
Contrast media is generally only needed if complications are suspected. CT scan should be done urgently in proptosis or impaired eye movement or vision because of orbital complications. CT scan should be done emergently if an intracranial spread of sinusitis is suspected due to severe headache, vomiting, or altered sensorium.3
Magnetic resonance imaging is not practical because of its high cost and sedation requirements. It can differentiate between the sinus secretion and mucosal thickening and between inflammation and malignant structures, and it is useful in chronic fungal sinusitis.3,19
Bacterial recovery is not recommended when deciding on management. Empiric treatment may be started once the clinical diagnosis of CRS is made. Nasal and postnasal discharge cultures are not reliable. Maxillary sinus puncture is the gold standard to retrieve relevant microorganisms; a drawback is that it reflects only the pathology in the maxillary sinus. It is an invasive and uncomfortable procedure performed only by otolaryngologists. To correctly identify pathogens in biofilm tissue, the sample needs to be analyzed with tests used only in research. Fungal cultures are never required in children because their form of fungal CRS is not invasive.9
When allergies or asthma are suspected, a full workup by an allergist is indicated, which may include an environmental assessment, skin tests, nasal provocation tests, and pulmonary function tests as deemed necessary. When immunodeficiency is suspected, immunoglobulins and lymphocytes need to be done. Investigations for GERD involve pH esophageal monitoring if symptoms suggest this condition. It is imperative to check for GERD before sinus surgery. For CF, a sweat chloride test should be done.
To diagnose mucociliary dyskinesia, a mucosal biopsy may be done, but no normal standard is established. A saccharin functional test may be performed.18,25,27,33
Treatment of CRS in children has a medical and surgical component. Initial therapy should be medical, except where obvious anatomic obstruction requires surgical relief.
Medical treatment should address both the inflammatory and the infectious component. CRS is now recognized as a multifactorial inflammatory disorder rather than a mere persistent bacterial infection. Nonetheless, sinus drainage is impaired in all forms of CRS, leading to secondary bacterial infections. Typically, repeat long-term courses of antibiotics are needed to treat acute relapses of CRS.1,3
Antibiotics are given over the long term for 3 to 6 weeks or more, until the patient is symptom free for 7 to 14 days. Short-term courses are inadequate. The antimicrobial agent covers a polymicrobial infection with aerobic and anaerobic bacteria that are shielded by the biofilm structure, exhibit certain resistance patterns, and produce beta-lactamase. Taking these issues into consideration allows effective empiric use of antimicrobials, despite the lack of reliable culture/susceptibility results in most cases. In the future, polymerase chain reaction testing on biofilm tissue may lead to more accurate identification of pathogens to guide therapy.
Studies showed amoxicillin-clavulanic acid or cefuroxime axetil provide good first-line treatment.8 Macrolides, with anti-inflammatory effects in addition to their antibacterial activity, may be better than other classes of antibiotics in treating biofilm. These data were mostly gathered from adult studies, and only inferences can be made for pediatric CRS.15
Clindamycin, quinolones (levofloxacin, moxifloxacin), and cephalosporins other than first generation have all been successfully used. Intravenous antibiotics in long courses achieved 100% effectiveness in some children with refractory CRS.35 Second- and third-generation cephalosporins do not eliminate interfering bacteria with their purported beneficial effects.14,21
Parenteral carbapenems offer coverage for most potential anaerobe and aerobe pathogens. For methicillin-resistant S aureus, a clindamycin and sulfamethoxazole-trimetoprim combination was reported to be effective.14 Fluoroquinolones (only in post-pubertal patients) are administered for P aeruginosa in CF.14 In immunedeficiency, CF, and primary ciliary dyskinesia, chronic preventative antibiotics may be given in conjunction with intravenous immunoglobulin treatments. The effectiveness of topical antibiotics and antifungals has not been proven, and, based on the current data, these medications are not recommended in pediatric CRS.1
Nasal steroid sprays are being widely used to decrease inflammation inherent to CRS, based mostly on anecdotal evidence. However, a recent literature review confirms they provide a modest benefit.1,18 Some preparations have been reported to reduce linear growth, at least temporarily.36
Mometasone furoate is the only intranasal corticosteroid approved for patients aged 2 years and older. This drug has no long-term effect on growth or the pituitary axis. Fluticasone propionate is approved for patients older than 4 years.
Oral corticosteroids are probably safe and effective when given in short bursts for severe symptoms of CRS; repeated or prolonged use significantly enhances the risk of side effects.37
Adjunctive therapies in children include oral antihistamine if allergy is present. In the absence of allergies, antihistamines are not used to treat bacterial sinusitis because they can thicken and dry secretions.
Saline nasal washes remove crusts, infective agents, and inflammatory mediators; liquefy secretions; act as a mild vasoconstrictor on nasal blood flow; and provide symptom relief. They show consistent evidence of benefit and are recommended as adjunct in the therapy of CRS.9,38 Nasal saline washes at concentration of isotonic saline (0.9%) or hypertonic saline are either commercially available or homemade solutions (Table 2).
Preparation and Use of Common Regimen of Nasal Saline Solution
Thermal water (sulfate-sodium chloride) inhalations were reported to induce a downregulation of inflammatory mediators in the nasal mucosa of children with CRS.39
Oral mucolytics, such as guaifenisin, may benefit symptoms of CRS. An effective expectorant, its use remains empiric in CRS. It has no side effects and it is recommended for symptomatic relief.9 Antileukotrienes have no proven efficacy in CRS.26
Preventing and treating comorbid conditions includes antireflux therapy in GERD30,32 and environmental control for allergens, smoke, and pollutants exposure.40
Antibiotic-associated diarrhea occurs in 11% to 31% of children treated with antibiotics.41 The potential role of probiotics in reducing the risk of this complication has been studied with increasing interest. Although inconclusive results exist, some studies and meta-analyses found evidence that probiotics given during antibiotic therapy, either as single agents (ie, Lactobacillus) or as yogurt containing active bacterial culture, significantly decreased the incidence of diarrhea in these children.42,43 They are safe to be used except in patients with a compromised integrity of the barrier of the intestine, those with short gut syndrome, the immunocompromised, and patients with central venous catheter. A large proportion of recently surveyed gastroenterologists confirmed they recommend probiotics in selected patients taking antibiotics.44
Surgery is rarely indicated and should be considered a last resort in the pediatric population.3,33 Adenoidectomy is the first-line surgical step to remove the reservoir of biofilm for chronic sinus infection. Functional endoscopic sinus surgery is done to enlarge natural ostia and to correct anatomic deformities having an effect on CRS. It may be considered when there is no improvement with maximal medical therapy, in failed adenoidectomy, in CF, in ciliary dyskinesia, and in patients with immunodeficiency (HIV/AIDS, chemotherapy-induced immune deficiency, and allergic fungal sinusitis). There are concerns of hindering midface growth in children undergoing this procedure, although data are conflicting.9,30,32
Treating CRS in children is difficult, with frequent relapses and failures. The regimens used are controversial, and measuring the effectiveness of any treatment depends on the type of assessment used. Traditional evaluation of objective outcomes should ideally be associated with a report on the results of therapy by children and parents.45
When to Refer a Patient with CRS
The management of pediatric CRS requires collaboration between pediatricians, allergists, otolaryngologists, pulmonologists, infectious disease specialists, gastroenterologists, and sometimes neurosurgeons. Specialist consultation should be sought when:
- The allergic or immunologic basis of a case of CRS needs to be clarified;
- There is refractoriness to appropriate treatment;
- There are frequent exacerbations that will severely affect the child’s quality of life and performance;
- There are opportunistic infections and symptoms and signs suggestive of CRS complications; or
- Comorbid factors need further assessment (eg, GERD) and complications occur (eg, intracranial extension).
Pediatric CRS may present with subtle, nonspecific disease not always matching the criteria of diagnosis established for adults. It is a multifactorial disease that requires a comprehensive, sometimes multidisciplinary approach. As a biofilm infection, CRS needs therapy that takes into consideration this particular nature. Use of probiotics in conjunction with antibiotics in selected patients may reduce the risk of antibiotic-associated diarrhea.
Our understanding of the role of predisposing/comorbid factors is evolving. The concept of local rhinitis may change the thinking about the involvement of allergy in CRS. Appropriate workup should take these factors into consideration as clinically indicated. Histopathology data may indicate that there is progression in the severity of tissue damage in time and that early diagnosis and treatment may prevent this progression.
Obtaining more knowledge on local innate immunity may open new avenues for management of this challenging disease.
- Fokkens WJ, Lund VJ, Mullol J, et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2012. Rhinol Suppl. 2012;(23):3 p preceding table of contents, 1–298.
- Silviu-Dan F. Pediatric chronic rhinosinusitis: the old, the new, and the reasonable. Pediatr Ann. 2011;40(4):213–220. doi:10.3928/00904481-20110316-09 [CrossRef]
- Tan R, Spector S. Pediatric sinusitis. Curr Allergy Asthma Rep. 2007;7(6):421–426. doi:10.1007/s11882-007-0064-5 [CrossRef]
- Tan BK, Rakesh KC, Pollak J, et al. Incidence and associated premorbid diagnoses of patients with chronic rhinosinusitis. J Allergy Clin Immunol. 2013;131(5):1350–1360. doi:10.1016/j.jaci.2013.02.002 [CrossRef]
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- Sidell D, Shapiro NK, Bhattacharyya N. Obesity and the risk of chronic rhinosinusitis, allergic rhinitis and acute otitis media in school-age children. Laryngoscope. 2013;123(10):2360–2363.
- Thomas M, Yawn BP, Price D, et al. EPOS Primary Care Guidelines: European Position Paper on the Primary Care Diagnosis and Management of Rhinosinusitis and Nasal Polyps 2007: a summary. Prim Care Respir J. 2008;17(2):79–89. doi:10.3132/pcrj.2008.00029 [CrossRef]
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- Desrosiers M, Evans GA, Keith PK, et al. Canadian clinical practice guidelines for acute and chronic rhinosinusitis. Allergy Asthma Clin Immunol. 2011;7(1):2. doi:10.1186/1710-1492-7-2 [CrossRef]
- Schleimer RP, Kato A, Peters A, et al. Epithelium, inflammation, and immunity in the upper airways of humans: studies in chronic rhinosinusitis. Proc Am Thorac Soc. 2009;6(3):288–294. doi:10.1513/pats.200808-088RM [CrossRef]
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- Coffinet L, Chan KH, Abzug MJ, Simões EA, Cool C, Liu AH. Immunopathology of chronic rhinosinusitis in young children. J Pediatr. 2009;154(5):754–758. doi:10.1016/j.jpeds.2008.11.035 [CrossRef]
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Diagnosis of Pediatric CRS
|Presenting CRS Symptoms in Children
|CRS Major Criteria:
Nasal Discharge (anterior or posterior drip)
- With or without cough
- With or without facial pain/pressure
|Other CRS Symptoms:
Very young: irritability, fatigability, poor eating
Young: gagging on mucus and vomiting from coughing;
Poor sleep, snoring, abnormal sleep positions, apnea
Sore throat on awakening, epistaxis
Older: malaise, sleep deprivation, decreased attention span, poor school performance
Any age: disguise as upper respiratory infections, otitis media, slow growth
Less frequently: fever, headache, halitosis, reduction/loss of smell
|Objective CRS Findings
Either signs on physical examination and/or relevant changes on computed to mography scan
Preparation and Use of Common Regimen of Nasal Saline Solution
One-half teaspoon salt (about 3 g) with 250 mL of boiled water (percentage of NaCl is 0.9%)
Optional: 1 teaspoon baking soda
|Preparation, Use, and Storage
Measure salt and, if used, baking soda and mix in clean cup. Add previously boiled water while still warm. Cool to room temperature. Fill clean dispensing device (eg, squeezing bottle, syringe) with solution. Rinse the nose two to four times a day. Do not put the used syringe, and do not plunge the used bottle tip, back into the solution while there is still solution in the cup because this will contaminate the remaining solution.
If a nasal steroid spray is also used, always use the salt and water mixture first and never immediately after the steroid spray because you may wash out the medicated spray too fast.
The mixture may cause mild burning sensation the first few times it is used; if this does not disappear in a few days, reduce the amount of salt.
Store any unused solution in a closed, clean container in the refrigerator for 1 to 2 days, then make a new solution. Discard any cloudy remaining solution. Wash the container with a mild soapy solution between uses.