Article #	2224
Journal	Rhinology 58 - 3
Article Title	Autonomic dysfunction as an independent risk factor for uncontrolled inflammation in chronic rhinosinusitis following functional endoscopic sinus surgery
Abstract	BACKGROUND: Chronic rhinosinusitis (CRS) is a multi-factorial disorder that causes systemic symptoms beyond rhinologic symptoms alone. A possible association between autonomic nervous system (ANS) dysfunction and CRS has been identified; however, few studies have confirmed this observation. In this study, we prospectively measured changes in ANS dysfunction symptoms following functional endoscopic sinus surgery (FESS) and explored the impact of ANS dysfunction on surgical outcomes of CRS. METHODOLOGY: Patients diagnosed with CRS who consented to surgical intervention were included prospectively. All patients completed the Sino-nasal Outcome Test-22 (SNOT-22) and the 31-item Composite Autonomic Symptom Score (COMPASS 31) questionnaires before the operation and during the follow-up period. Clinical demographic data, Lund-Mackay, and modified Lund-Kennedy scores were recorded and measured. RESULTS: A total of 102 patients were enrolled. The median SNOT-22 and COMPASS 31 scores significantly improved following FESS from 43.0 to 14.0 and 21.0 to 11.2 (all P less than 0.001), respectively. FESS led to a significant reduction in the prevalence of various ANS dysfunction symptoms. In multivariate analyses, revision surgeries (odds ratio [OR] 5.012, 95% confidence interval [CI] 1.52416.489; P=0.008), CRS with nasal polyps (OR 4.071, 95% CI 1.454-11.40; P=0.008), and higher Pre-FESS COMPASS 31 scores (OR 1.043, 95% CI 1.003-1.084; P=0.036) were independent risk factors for uncontrolled inflammation following FESS. CONCLUSIONS: ANS dysfunction symptoms are prevalent in CRS and higher preoperative COMPASS 31 scores correspond with poor surgical outcomes. Following FESS, the majority of ANS dysfunction symptoms can be alleviated. Further investigations are required to explore the possible mechanism of how ANS is involved in the pathogenesis of CRS.
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