Medical management of chronic rhinosinusitis

Abstract

Appropriate medical management of chronic rhinosinusitis (CRS) requires a thorough understanding of the dynamics of the disease process, which is often multifactorial. Furthermore, the spectrum of factors at work in any individual patient varies depending on medical comorbidities, atopic status, whether the patient has had sinus surgery, and regional geographic variations. As for any other local or systemic inflammatory disease, treatment outcomes in CRS certainly depend on the patient's general medical condition. This aspect mandates diagnosis and management of diabetes and any immunodeficiency, as well as control of air quality and smoking cessation. Unfortunately, however, the dominant driving force behind the chronic inflammatory process is often idiopathic, and a final common biochemical pathway is yet to be elucidated. Nonetheless, it is clear that the pathophysiology is far more complex than merely representing a prolonged bacterial infection or a simple allergic phenomenon. CRS as a pathological process is better understood as a chronic inflammatory disease rather than an infectious disease, although microorganisms do play a significant role in the progression and exacerbation of the condition. The clinical syndrome of CRS, as has been defined elsewhere in this text, may be further described according to phenotypic presentation as CRS with nasal polyps (CRSwNP) or CRS without nasal polyps (CRSsNP). Prevailing thought is that these entities represent distinct disease processes, whereby CRSwNP tends to demonstrate a T-helper 2 (Th2) cytokine profile [interleukin (IL)-4, IL-5, IL-13] and eosinophilic inflammation, while CRSsNP tends to exhibit a T-helper 1 cytokine profile and neutrophilic inflammation. This distinction may also have therapeutic implications. A number of metabolic, genetic, or inflammatory disease states may be associated with the syndrome of CRS, including various immunodeficiencies, cystic fibrosis (CF), aspirin sensitivity triad (asthma, aspirin allergy, and rhinosinusitis/ nasal polyposis), ciliary diskinesia, and allergic fungal sinusitis (AFS). Phenotypic characterization, as well as recognition of underlying disease processes, is critical in the selection of appropriate medical therapy. Multiple theories have been proposed for the development of CRS (with or without nasal polyps) in the absence of definable underlying conditions. These ideas address the roles of atopy, osteitis [1], bacterial biofilms [2], bacterial superantigens [3], and defects in innate immunity [4]. Others have even demonstrated that fungi may stimulate the cascade immune responses seen in some patients with CRS, in the absence of florid AFS. In any individual patient, one or more of these processes may be at work. The present chapter addresses medical management of the CRS patient, with or without polyps, in the context of known and hypothesized pathophysiologies of the disease process. Although a standardized algorithm or a "one size fits all" approach cannot be applied in the management of CRS, our state of knowledge to date does permit definition of key treatment principles. Medical treatments can broadly be divided into agents that address the target of the inflammatory reaction (particularly antimicrobial therapy) and agents which modulate the inflammatory reaction itself (immunomodulatory therapies). © 2008 Springer Science+Business Media, LLC. All rights reserved.