xRead - Nasal Obstruction (September 2024) Full Articles

20426984, 2021, 3, Downloaded from https://onlinelibrary.wiley.com/doi/10.1002/alr.22741 by Stanford University, Wiley Online Library on [01/07/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License

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International consensus statement on rhinosinusitis

Lien et al. 790 demonstrated an increased incidence of frontal sinusitis associated with cells that affect the posterior or posterolateral aspect of the frontal recess (suprabullar, supraorbital, and frontal bullar cells) with no association found with frontal cells. Langille et al. 791 showed a significant relationship between the presence of frontal cells and mucosal thickening on CT imaging. In contrast to these studies showing an association between anatomic variants and sinonasal disease, there is also a significant body of literature that does not demon strate a relationship. Nouraei et al. 784 and Bolger et al. 348 found no relationship between anatomical variations of the middle turbinate or other structures that could affect the OMC and impact on Lund-Mackay score. Cho et al. 340 noted no correlation between middle turbinate variations or NSD and presence of sinus inflammation on CT scan. Similarly, articles by Shpilberg et al. 334 and Balikci et al. 792 found that anatomic variants such as concha bullosa, NSD, and agger nasi cells are common, but not associated with CRS. Kalaiarasi et al. 793 also demonstrated that concha bullosa was not associated with ipsilateral CRS except in the case of extensive conchae. In 2 studies focusing on the frontal sinuses of patients with a history of CRS, the presence of frontal recess cells and agger nasi cells were not associated with a higher incidence of frontal sinusitis. 794,795 Additionally, no association was found by DelGaudio et al. 795 between frontal sinusitis and size of the frontal recess. When specifically studying frontal sinus anatomy, DeConde et al. 796 showed that the frontal sinus outflow dimensions, presence of intersinus septal cell, and an anterior ethmoid artery on a boney mesentery did not impact QoL gains from endoscopic frontal sinus surgery. In conclusion, there is literature both supporting and refuting an association between anatomic variations and CRSsNP. The articles demonstrating an association show a generally small effect with some contribution of anatomic variation in the disease process. Overall this suggests a small, if any, role of anatomic variations in the pathogene sis of CRSsNP.

IX.C.10 Contributing Factors for CRS: Septal Deviation Because of limited data, CRSsNP and CRSwNP are com bined in this analysis. Since the publication of ICAR-RS-2016, nasal septal deviation (NSD) as a contributing factor to CRS has been considered in several studies. The largest, published in 2016, analyzed the data from the Korean National Health and Nutritional Examination Survey (years 2008-2012) which was aimed at determining the prevalence and risk factors of CRS, AR, and NSD in Korea. Ahn et al. 23 enrolled 35,511 subjects and performed an interview regarding nasal symptoms and a nasal endoscopic examination. Afterward the subjects were divided into 3 age groups: children (aged 7-12 years), adolescents (aged 13-19 years), and adults (aged ≥ 20 years). CRS was classified as CRSwNP and CRSsNP, and its prevalence was estimated in adults according to the EPOS 2012 guidelines on the basis of symptoms and/or nasal endoscopic findings. NSD was evaluated via nasal endoscopy after nasal decongestion in the adolescent and adult groups. When obstructive symptoms were present for more than 3 months, NSD was defined as symptomatic. In this study, the prevalence of NSD combined with CRS was estimated at 4.3%, with a prevalence of 1.2% and 3.1% for CRSwNP and CRSsNP respectively. After adjusting the results for risk factors of adult CRSsNP, NSD still increased the risk for CRSsNP, while it did not increase the risk for CRSwNP. In 2018 Sohn published a prospective case series of 304 patients aged ≥ 18 years, affected by either RARS, CRSsNP, orCRSwNP. 509 All of them were evaluated for clinical pre sentation and anatomic variants using preoperative CT. Differences in the postoperative improvement of each cat egory according to the results of the SNOT-20 survey were reported. A significantly greater prevalence of anatomic variants, such as agger nasi cells, Haller cells, and NSD were found in the RARS group with an NSD prevalence of 86.5%. NSD was present in 41.5% of CRSsNP and 56.3% ofCRSwNP. 509 Fu et al. 799 published a case control retrospective study on patients undergoing revision ESS between January 2010 and December 2017 for CRS, as defined by the clinical practice guideline of the AAO-HNS. Patients were defined as eligible for revision ESS if appropriate medical ther apy failed and radiographic evidence of persistent disease was found. In total, 489 patients underwent revision ESS. The authors reported that untreated NSD was significantly associated with radiographic markers of CRS severity and likely represents one of many local factors contributing to the multi-factorial pathogenesis of CRS. They there fore recommended correction of clinically significant NSD

Anatomic Variations as a Contributing Factor forCRSsNP Aggregate Grade of Evidence: D (Level 3: 2 studies; level 4: 19 studies; Table IX-11). Results of studies are conflicting.