xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

studies have identified bacteria in the bone specimens. 644–646 Topical antibiotic irrigations were also trialed in animal models, but demonstrated no impact on bone histopathology. 674 In conclusion, the role of neo-osteogenesis in the patho physiology, propagation, and recalcitrance of CRS has yet to be definitively determined. Additional research is required to investigate causality and not just association with the severity of CRS.

who illustrated higher SNOT-20 scores in CRS patients with GERD compared to those with only extra-esophageal symptoms of reflux (Mean 19.3 vs 7.4, p < 0.005) and a prolonged saccharin test demonstrating delayed nasal mucociliary transport time in the study group. 691 Not all data implicates direct acid or non-acid exposure in CRS pathophysiology. Jecker et al. found that in 20 surgi cally refractory CRS patients there were significantly more reflux events in the distal pH probe when compared to the 20 healthy controls. 683 CRS patients additionally had a higher DeMeester index (32.9 + / − 8.7 vs 6.6 + / − con trols), and the patients’ esophageal mucosa was exposed to gastric acid for a mean of 95 minutes during the record ing period relative to 16.6 + / − 4.6 minutes in controls. However, the location of the reflux events was somewhat paradoxical; with greater than 10 times more events in the esophagus (95.5 + / − 31.0) relative to the hypopharynx (8.5 + / − 2.5) ( p < 0.01). This data gives credence to an alter native mechanism to explain sinus inflammation in the absence of direct acid injury, such as a vagally mediated reflex - the so-called esophagonasal reflex . 692 This was fur ther explored by Wong et al., who analyzed the nasal symp toms of 10 healthy volunteers after esophageal infusion of hydrochloric acid (HCl). 693 The infusion of HCl led to a non-significant rise in mean symptom score, as well as a reduction of nasal patency as measured by nasal inspira tory peak flow. Of the 267 recorded reflux episodes, none reached the nasopharynx. Ozmen et al. found a higher rate of pharyngeal acid reflux events (PARE) using dual probe pH monitoring in the pharynx and LES in 29/33 CRS patients (88%) com pared to 11/20 controls (55%). 682 Specific pepsin activity was identified in 82% of the study group compared to 50% of controls ( p = 0.014). Loehrl et al. demonstrated reflux events at all tested sites, including the nasopharynx, in 20 medically refractory CRS patients. 694 The authors per formed nasopharyngeal biopsies of all subjects, with none testing positive for pepsin (0/20). However, in 5 subjects who underwent nasopharyngeal lavage, 100% were pos itive for pepsin, compared to zero of 5 healthy controls. DelGaudio examined medically and surgically refractory CRS patients compared to controls. 676 He demonstrated that nasopharyngeal reflux events occurred in 39% of sur gically refractory patients compared with 10% of controls below a pH of 4, and 76% compared with 24% below a pH of 5. Reflux scores, CRS symptoms and SNOT-20 scores, and endoscopic examination scores were significantly higher in the study group. Gastric acid and protease exposure has been well estab lished as leading to dilation of the intercellular spaces in esophageal mucosa, with impaired mucosal integrity, and could be equally deleterious to upper airway mucosa. 695 DelGaudio postulates that nasal mucosa is susceptible

Neo-osteogenesis as a Contributing Factor for CRS Aggregate Grade of Evidence: C (Level 2: 7 studies; level 3: 12 studies; level 4: 5 studies; Table IX-6).

IX.C.5 Contributing Factors for CRS: Gastroesophageal Reflux Because of limited data, CRSsNP and CRSwNP are com bined in this analysis. Laryngopharyngeal reflux (LPR) is the retrograde dis persal of gastric contents into the upper airway. In the United States, the estimated prevalence of gastroe sophageal reflux symptoms ranges from 6% to 30%. 675 The pathophysiology linking LPR to CRS is unclear, although there appear to be several putative mechanisms suggesting that reflux disease may be a causal factor and an aggravat ing factor of CRS. The exposure of nasopharyngeal and sinonasal mucosa to injurious gastric contents has been stud ied in adults 676–686 with gastroesophageal reflux disease (GERD) identified as a significant risk factor for poor outcomes following ESS. 687 Ulualp and Toohill identified a high rate of pharyngeal acid reflux and overall reflux events in adult CRS patients vs controls. 688 Ulualp et al. confirmed a significantly higher prevalence of reflux in refractory CRS patients vs controls (7/11, 64% vs 2/11, 18%). 684 Pincus et al. corroborated this, finding 25/30 (83%) patients with refractory CRS had positive pH studies, with improvement in most evaluable patients treated with proton pump inhibitors (PPIs) over 1 month (14/15, 93%). 677 Conversely, the prevalence of CRS in patients with reflux/GERD was 20.7% (95% CI, 12.0-29.5%) (Bohnhorst et al. 2015). 689 Loerhl and Smith 677 postulate that reflux causes an autonomic reflex leading to an inflammatory response and impaired MCC. 690 This is supported by Delehaye,