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Page 2 of 9               Go et al. Plast Aesthet Res 2024;11:11  https://dx.doi.org/10.20517/2347-9264.2023.110

               significant physical, psychosocial, and emotional burdens. Thought to be a result of excessive turbinate
               reduction or resection during nasal or sinus surgery, ENS is a clinical entity with a spectrum of symptoms
               including nasal obstruction, dryness, burning, and feelings of suffocation. The exact incidence in turbinate
               reduction patients is currently unknown as there is a lack of primary literature reporting such data.
               Persistent empty nose syndrome symptoms can be distressing, requiring a nuanced and empathetic
               approach to diagnosis and management. There are a variety of different treatment options including both
               non-surgical and surgical methods involving reconstruction of the resected turbinate. A comprehensive
               review of ENS and suggested approach to management in post-rhinoplasty patients are discussed below.

               PATHOPHYSIOLOGY
               Located along the lateral walls of the nasal cavity are three pairs of turbinates which are the workhorse of
               nasal function, playing a key role in warming, humidifying, and filtering breathed air. As the most anterior
               turbinate pair, the inferior turbinates help regulate airflow through swelling and contracting in order to
               allow for proper flow rate and moisture levels within the nasal cavity. Pseudostratified ciliated columnar
               epithelium with goblet cells lines the sinonasal cavity and allows for rapid expansion and contracture
                                          [1]
               through autonomic stimulation . During the nasal cycle, which can last anywhere from thirty minutes to
               six hours, these structures alternate with each other so that only one turbinate is enlarged at a time .
                                                                                                 [2]
               Nasal microbiota plays a complex and essential role in regulating the mucosal immune system, which can
               play an important role in the histological expression in empty nose syndrome. Nasal dysfunction and
               reactive nasal inflammation may trigger a complex cascade of dysregulatory events, such as in diseases like
               chronic rhinosinusitis. Classically, disruption of the epithelial boundary allows for mucosal permeability
                                                                                                    [3]
               and bacterial penetrance, promoting Th-2 inflammation and the release of inflammatory cytokines . As a
               result of disruption to the mucosal barrier after turbinate surgery, patients may experience dysregulation of
               the mucosal immunity that can influence the overall histologic picture. One histopathology study found
               increased squamous metaplasia, submucosal fibrosis, and lower submucosal glands compared to controls .
                                                                                                        [4]
               The interactions of the nasal microenvironment in empty nose syndrome remain multifold and play an
               important role in the pathogenesis of this complex disease.


               Alteration in the nasal physiological pathway can cause inhaled air to flow directly through the nasal cavity
               to the nasopharynx, losing the turbulent airflow that humans usually perceive with their nasal breathing.
               The most common reason for turbinate impairment is iatrogenic injury. Surgical resection of the inferior
               turbinates during sinonasal procedures can lead to excessive tissue reduction in the nasal cavity, thus
               impeding the natural physiologic processes of moisturization and humidification. Additionally, impairment
               of mucosal function secondary to surgical and non-surgical insult may occur. Abnormal neural healing after
               surgery can result in improper sensory connections, thus leading to increased nasal sensitivity and pain .
                                                                                                        [5]
               Several studies  have demonstrated impaired menthol lateralization detection thresholds in patients with
                            [6,7]
               ENS compared to healthy controls - menthol, a trigeminal agonist, is presented in serially diluted amounts
               to patients, who must identify which bottle contains the reagent. Patients with ENS had lower thresholds,
               suggesting decreased trigeminal sensitivity to volatile compounds, which may contribute to a lack of
               perception of airflow with inhalation. A recent meta-analysis by Kanjanawasee et al. corroborated these
                                                                               [8]
               results, finding that menthol detection test was statistically impaired in ENS .
               A combination of these physiological changes can cause patients to experience the significant discomfort
               that is characteristic of ENS. It has been thought that ENS symptoms were more common in more arid
               regions of the world due to lack of environmental humidity, but it has more recently been believed that
               symptom severity was not inherently related to climate or geographic factors . Exacerbation of symptoms
                                                                                 [9]
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