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Introduction: There has been an explosion in the understanding of the mechanisms of chronic sinonasal inflammation. Multiple approaches to control and modify the inflammatory reaction in chronic rhinosinusitis have led to many new agents being introduced topically to the sinonasal cavities. This article aims to provide an evidence-based approach to the science behind topical management of sinonasal disease. Methods: The literature on delivery device, position, surgical state, and pharmaceutical and mechanical concepts of topical therapy to the paranasal sinuses is reviewed. Results: High-volume irrigation under positive pressure and in head-down positions is important for effective delivery and mechanical action of topical solutions. Unoperated paranasal sinuses appear to receive very limited topical therapy. Enhanced steroid therapy and surfactants appear to be the most promising pharmaceutical approaches. Future novel therapies may include enhancers of the innate immune system. The effect of antibiotic additives is difficult to establish as this might be treating a disease-modifying state rather than the underlying pathology. Conclusions: Topical therapies, applied after surgery, are likely to represent the mainstay of future management for chronic inflammatory rhinosinusitis. [ABSTRACT FROM AUTHOR]

Objective: Persistent pneumocephalus often indicates the presence of a skull base (SB) defect associated with one of the paranasal sinuses. Such defects require treatment to avoid sequelae. The study objective was to evaluate success in endoscopic closure of SB defects associated with pneumocephalus. Design: Retrospective medical record review. Setting: Tertiary care academic rhinology practice. Methods: A 5-year retrospective review of patients presenting with pneumocephalus. Presenting symptoms, etiology of SB defects, radiologic findings, operative techniques, and follow-up were evaluated. Main Outcome Measures: Success of endoscopic SB defect repair in the setting of pneumocephalus was assessed. Factors potentially contributing to failure were evaluated in appropriate cases. Results: Eleven patients with pneumocephalus from 14 SB defects underwent 17 endoscopic repairs. In 11 surgical procedures, active cerebrospinal fluid (CSF) leaks were identified, but in the remaining 6, pneumocephalus was present without CSF leak. Radiologic location of pneumocephalus ranged from extra-axial to diffuse within the brain parenchyma. SB defects were identified using fine-cut computed tomographic (CT) scans, CT cisternograms, and intrathecal fluorescein. Defects were located in the sphenoid, sella, ethmoid roof, and frontal sinus posterior table. Eight of 11 patients (72%) were managed with endoscopic repair alone. Factors potentially effecting failure included malignancy, previous radiation, intracranial infection, malnutrition, and Cushing disease. Conclusions: Endoscopic SB defect repair for pneumocephalus is largely successful. Localization of SB defects in these cases is often assisted by CT cisternography and intrathecal fluorescein. [ABSTRACT FROM AUTHOR]

Introduction: Chronic rhinosinusitis with nasal polyposis (CRSwNP) represents an eosinophilic T-helper 2 inflammatory response. Local production of IgE within nasal polyps (NPs) has been demonstrated, suggesting a role for local IgE in the pathogenesis of NP in atopic CRS patients. We hypothesized that local IgE specific to inhalant allergens may also play a role in the genesis of NP in nonatopic CRS patients. Methods: Sinus and inferior turbinate tissue was obtained from nonatopic CRSwNP patients (n = 7), chronic rhinosinusitis without nasal polyps (CRSsNP) patients (n = 15), and healthy controls (n = 9) at the time of surgery. ImmunoCAP analysis (Phadia AB, Portage, MI) for 14 common inhalant antigens was performed on tissue homogenates to determine the antigen-specific response. Results: Total IgE levels did not differ in sinus or turbinate tissue between CRSwNP, CRSsNP, or control patients. CRSwNP sinus tissue had higher levels of specific IgE for cockroach and plantain (p = .03) than other groups and elevated Alternaria IgE levels when compared with CRSsNP sinus tissue (p < .05). No significant differences were found for any of the other antigen-specific IgE levels. Fifty-seven percent of CRSwNP polyps demonstrated a polyclonal IgE response, whereas the other 43% had no demonstrable antigen-specific IgE. In contrast, only 17% of CRSsNP patients demonstrated a polyclonal response within sinus tissue, whereas 67% had no detectable antigen-specific IgE. There was no significant difference in levels of IgE in inferior turbinate tissue between the groups (p < .05). Conclusions: Localized mucosal IgE specific to common inhalant allergens appears to play a role in a subset of CRSwNP patients without evidence of systemic atopy. [ABSTRACT FROM AUTHOR]

Following publication of the original article [1], the authors reported an error in Table 1. In the second columns of the 'Radiology' row, 'Normal anterolateral sinus mucosa' should read 'Normal superolateral sinus mucosa'. A corrected version of Table 1 is included in this Correction. [ABSTRACT FROM AUTHOR]

Background: Chronic rhinosinusitis (CRS) is a complex disease that incorporates many different conditions. Currently, primary CRS is considered a disease of broad airway inflammation, however, the previous classification of CRS with and without nasal polyposis fails to adequately classify patients based upon their etiology of illness. Our aim with this review is discuss the clinical presentation, radiology, endoscopy, histopathology, and treatment algorithm of three different phenotypes of primary CRS: central compartment atopic disease, eosinophilic CRS, and non-eosinophilic CRS. Methods: A narrative review of a tertiary rhinology center's research themes and how they are applied to clinical protocols and practice was assessed. Discussion: Diagnosis and treatment of upper and lower airway conditions become increasingly important as phenotypes and endotypes are being described. There are well-described therapies to treat the different phenotypes of CRS, based upon the presumed underlying cause of the inflammatory process. Research continues to shed more light on different endotypes and phenotypes of airway inflammation, however, clinical differentiation of CRS can be applied in clinic practice with three simple phenotypes of CRS. Understanding these different phenotypes and their etiologies allows for further management beyond the 'maximum medical therapy and then surgery' approach that has often been used in the management of CRS. [ABSTRACT FROM AUTHOR]