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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disease. Similarly, Khojastepour et al. 333 found that infraor bital cells are associated with maxillary mucosal disease on cone beam CT scan in patients presenting for rhinoplasty evaluation. In addition, other studies have demonstrated that sphenoethmoidal cells (Onodi cells) may be associated with radiographic sphenoid mucosal thickening, again, ostensibly from narrowing of the natural sinus ostia. 787 Jain et al. 338 performed a retrospective cohort study and compared groups with limited sinus disease, pansi nusitis, and a control group without sinonasal disease. The authors examined CT sinuses and found a signifi cantly higher average number of anatomical anomalies (accessory ostia, conchae bullosae, infraorbital ethmoid cells, lateralized uncinate processes, and paradoxical mid dle turbinates) in patients with limited sinus involvement on CT compared to the other cohorts. Specifically, the authors found that the group with limited sinus disease had 96 anatomic variations in 22 patients, while the con trol group had 68 variants in 27 patients, and the pansi nusitis group had 72 variants in 28 patients ( p = 0.003). They proposed that these anatomical variants cause lim ited disease when they impair function of the OMC while a primary mucosal abnormality is responsible for individ uals with more global disease. In a similar study the same group demonstrated that in cohorts undergoing anterior ESS only or ESS for CRSsNP or CRSwNP that the patients undergoing surgery for CRSsNP and anterior ESS were more likely to have anatomic variants than the CRSwNP cohort, supporting again the idea that CRSwNP is a more global disease process and that anatomic factors may play a role in more limited disease. 788 In another surgical study, Qualliotine et al. 789 found that patients with con cha bullosae had worsened QoL scores and improved more after surgery than patients without that specific anatomic abnormality. Sedaghat et al. 785 found sinonasal anatomic variants (concha bullosae, intersinus frontal cells, frontal air cells and infraorbital ethmoid cells) predispose to progression to CRS over time in patients with underlying AR. In this study the authors performed a retrospective review of a cohort of patients initially diagnosed with AR, who had follow up of at least 4 years. They found that a signifi cant proportion progressed to develop CRS, and examined the factors that contributed. Among other factors, such as asthma, anatomic variants were associated with faster progression to the development of CRS. This study is lim ited by the retrospective design, and the relatively small sample size as only 24 patients were identified that pro gressed from AR to CRS, but the authors concluded that anatomic narrowing may promote development of inflam mation in the sinuses and development of CRS in AR patients.

enrichment of a particular organism has been uniformly identified. There is considerable interest in the functional relevance of the microbial community that may contribute to sinus health or disease. Further investigations of the sinonasal microbiome may promote better understanding of CRS, leading to novel therapeutic interventions with potential opportunity for personalized medicine.

Microbiome Disturbance as a Contributing Factor for CRS Aggregate Grade of Evidence: C (Level 3: 4 studies, Level 4: 4 studies; Table IX-10).

IX.C.9 Contributing Factors for CRSsNP: Anatomic Variation There are a multitude of sinonasal anatomic varia tions that are described and may theoretically con tribute to the pathology of CRS. These variations are generally thought to narrow anatomic drainage path ways, such as the frontal sinus or the osteomeatal complex. 332,338–340,342–343, 346, 348,780–786 Examples of sinonasal variants include infraorbital (Haller) cells, concha bullosae, paradoxical curvature of the middle turbinates, nasal septal deviation (NSD), suprasphenoid ethmoidal cells (Onodi), and frontal sinus variations including frontal sinus cells, supraorbital cells, suprab ullar cells, frontal bullar cells, and intersinus septal cells. These variants are often present in the general population as well, suggesting that variations alone may not cause pathology without other factors. Additionally, underlying disease processes may also contribute to variation. For example, maxillary pathology may lead to medial displace ment or thinning of the uncinate process, which could be interpreted as contributing to the disease process, when, in fact, the variation may result from the disease process. Multiple studies have described an association between anatomic variation and development of CRSsNP. Caughey et al. 342 found patients with infraorbital ethmoid cells had overall increased Lund-Mackay CT scores for the frontal, ethmoid, and maxillary sinuses, but only the ethmoid and maxillary sinuses had increased scores when comparing individual sinuses. In the same study, patients with a con cha bullosa had increased Lund-Mackay scores for max illary sinuses only. The form of RS (CRS vs ARS) was not delineated, but the study suggests that obstruction of the OMC can lead to ethmoid and maxillary mucosal