Etiology, Diagnosis and Management of Chronic Rhinosinusitis

R Peter Manes; Pete S Batra


Expert Rev Anti Infect Ther. 2013;11(1):25-35. 

In This Article

Abstract and Introduction


Chronic rhinosinusitis (CRS) is a common health care problem, yet many aspects of this diagnosis remain poorly understood. Its etiology is often debated and remains a significant area of research. The diagnosis of CRS is based on subjective symptoms, duration of symptoms and objective evidence of inflammation. Each of these criteria must be met to make a diagnosis of CRS. Management of CRS often involves a combination of systemic and topical therapies with surgery reserved for patients who fail medical therapy. This review provides a comprehensive view of the etiology, diagnosis and management of CRS.


Chronic rhinosinusitis (CRS) represents one of the most common healthcare problems in the USA, afflicting approximately 31 million Americans.[1] CRS is a clinical syndrome associated with persistent inflammation of the mucosa of the nose and paranasal sinuses for 12 weeks or longer.[2,3] It is known to cause significant physical impairment, adversely impacting patient quality of life and psychosocial well-being. Despite its prevalence, CRS remains a challenging and, at times, controversial, disease entity. The etiologic mechanisms of CRS continue to be a source of much debate and, as such, different schools of thought exist on the optimal management strategy. The purpose of this review is to describe the different proposed pathophysiologic mechanisms of CRS as well as review the diagnostic and treatment strategies for the management of this complex disease.

Accurate diagnosis of CRS rests on the ability to identify signs and symptoms associated with the disease process, such as nasal obstruction, purulent discharge and/or facial pain, as well as objective evidence of mucosal inflammation, either by nasal endoscopy and/or computerized tomography.[4] However, it is also important to recognize that this is a heterogeneous disease spectrum subject to further subclassifications. Patients with CRS may be divided between CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). This distinction leads to both clinical and pathological differences. CRSwNP is predominantly mediated by eosinophils, as well as increased levels of histamine, IL-5 and IL-13.[5] By contrast, CRSsNP seems, at first glance, to be predominantly mediated by neutrophilic inflammation.[6] However, some CRSsNP cases may also exhibit extensive eosinophilic infiltration. Therefore, the distinction between CRS with and without polyps is not as clear as originally thought. In addition, CRS must be clearly differentiated from systemic processes that lead to sinonasal mucosal inflammation. Clinical entities, such as cystic fibrosis, sarcoidosis, Wegener's granulomatosis and primary immunodeficiency (PID) may present with sinus involvement as a component of the multisystem process. Some cases of PID can be relatively mild and manifest primarily as sinusitis without pneumonia or other more serious systemic infections. The prevalence of PID in patients with recalcitrant CRS varies widely in the literature, from 0 to 19%. Furthermore, secondary CRS may arise as a result of local, discrete processes such as tumor, mycetoma and foreign body reaction. A recent study even suggests a potential causal relationship between tobacco smoke exposure and the development of CRS.[7] The primary focus of this review is to discuss CRS as a primary disease process in the absence of systemic or local predisposing factors.